Gram positive bacteria – Enterococcus

What are Gram positive bacteria – enterococci?

Enterococci are ubiquitous gram-positive cocci, calatase-negative, non-spore-forming, facultative anaerobic organisms, that belong to the Lancefield group D streptococci.

Enterococci are normally present, as colonizers, in the intestinal tract of human beings and animals, and can be recovered from feces in large quantities. Enterococci may occasionally reside in the vagina and oral cavity. They also may be found in food and water.

The two predominant enterococcal species in humans are E. faecalis and E. faecium, while other species are occasionally found.

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Enterococci may survive in adverse environmental conditions, such as high temperature, drying, and in some antiseptic agents. This property helps enterococci contaminate surfaces and medical equipment, enabling it to be transmitted to patients via healthcare workers, causing outbreaks.

Although enterococci have been considered a low-virulent pathogens, during the last decades they have become an important cause of a variety of infections that primarily affect debilitated and immunocompromised patients and are mainly hospital-acquired or healthcare associated infections.

High-level resistance in enterococci to antibiotics such as betalactams, aminoglycosides and glycopeptides has increased dramatically in the last three decades and the treatment of some enterococcal infections has become a challenge for clinicians.

The changing epidemiology of enterococcal infections necessitates that the microbiology laboratory identify enterococci at the species level because the enterococcal species may have different epidemiology and antibiotic resistant patterns.

Importantly, recent studies have disclosed the genomics of enterococci, particularly E. faecalis and E. faecium, providing new insights to better understand the biology of enterococci. Comparative genomic analyses have exhibited considerable intra-species genomic diversity also within clonally related strains, which is mainly linked to the variable presence of plasmids, phages, pathogenicity islands and conjugative elements.

Also, reports on experimental models in animals have evaluated the host immune response against enterococci and have given some insights about the increased vulnerability of immunocompromised and critically ill patients to enterococcal infections.

Most putative virulence determinants associated with E. faecalis(and less frequently with E. faecium) are involved in adherence to extracellular structures and biofilm formation, which appear to be important factors for colonization and infection. Mobile genetic elements such as plasmids and transposons are crucial to the spread of antibiotic resistance in enterococci and also to transfer resistance determinants to other bacteria such as Staphylococcus aureus.

With the next generation of sequencing approaches such as pyrosequencing, with lower cost and higher performance, many more enterococcal genomes will be sequenced, and our understanding of the enterococcal virulence determinants and enterococcal biology will increase.

However, little is known about the adaptive response mechanisms of enterococci to several conditions.

New advances in genomics including the knowledge of the enterococcal virulence determinants and the adaptive response mechanisms of enterococci to different conditions as well as a better understanding of the host immune response to these pathogens will be able to create new approaches for reducing colonization and infection as well as novel therapeutic alternatives for difficult-to-treat enterococcal infections.

Enterococcal infections

Enterococci are relatively low virulence organisms, but they can invade the debilitated and immunocompromised host and cause a variety of serious infections.

Although enterococci can produce community-acquired infections, in recent years there have been an increased number of enterococcal healthcare associated infections (HAI). Enterococci are often involved in mixed infections. Enterococcal healthcare associated infections are often preventable and cause poor outcomes and increased costs.

Enterococci can harbor intrinsic low-level antibiotic resistance. Moreover, in recent years, enterococci have developed an escalating process of acquiring high-level antibiotic resistance to aminoglycosides, beta-lactams and glycopeptides.

High-level resistance to gentamicin, streptomycin or both has been observed in the US and Europe, and may affect both E. faecalis and E. faecium. The main clinical consequence of high-level aminoglycoside resistance is the lost of synergistic effect when adding to ampicillin or vancomycin in endocarditis or other serious enterococcal infections.

High-level resistance to betalactams and glycopeptides is of special concern, and both resistance patterns are mainly concentrated in E. faecium.

Although the figures for high-level ampicillin resistant are quite similar in the US and Europe, there are clear differences in the epidemiology of glycopeptide resistance in enterococci

High-level glycopeptide resistance is most commonly associated with vanA gen cluster and generates resistance to vancomycin and cross-resistance to teicoplanin. A great problem in clinical practice is that glycopeptide resistance can be transmitted intra-species and inter-species.

To find the most appropriate therapeutic option for enterococcal infections with high-level resistance to ampicillin and vancomycin is a complicated issue and may requiere new agents.

Prevention of vancomycin-resistant enterococci (VRE)

The emergence of vancomycin-resistant enterococci (VRE) has become a major problem in many healthcare institutions and, therefore, control and prevention of infection and colonization with VRE have become imperative. Most preventive strategies for VRE are also applicable to other antibiotic-resistant enterococci.

Preventing VRE colonization of the intestinal tract is essential, since it usually precedes the infection. Patients receiving antibiotics may have increased density of VRE colonization and VRE in stools which may increase and facilitate their dissemination. VRE may spread from patient to patient through the healthcare workers (with poor hand hygiene practices and insufficient compliance with contact precautions) and may contaminate the surfaces and medical equipment.

In brief, several risk factors for infection and/or colonization with VRE have been identified. These include:

  • Patient characteristics and site of care

  • Prior antibiotics

  • Colonization pressure and

  • Environmental contamination.

One important issue for an infection control team is to prevent transmission of VRE in the healthcare settings. These strategies include:

  • Hand hygiene, contact/barrier precautions, and source control.

  • Cohorting of colonized/infected patients and/or healthcare workers such as nursing staff; use private rooms when possible.

  • Surveillance studies for detecting colonization.

  • Prudent use of antibiotics.

  • Environmental cleaning programs in hospitals to optimize cleaning of high touch surfaces and medical equipment.

Current controversies

There are several controversial issues and questions regarding enterococci that are not fully answered. These include:

  • What are the genetic and molecular mechanisms that really lead to an increased pathogenicity and virulence of enterococci?

  • What are the host response mechanisms effective in preventing enterococcal infection?

  • What is the role of genetic and molecular determinants that may cause and facilitate spreading antibiotic resistance in enterococci?

  • What is the best methodology for improving and evaluating the hand hygiene practices and barrier precautions compliance in different healthcare settings?

  • How can a health care institution really improve the prudent use of antibiotics?

  • What is the effectiveness of a program using active surveillance cultures and subsequent isolation of colonized patients to control VRE?

  • Can the administration of drugs suppress or diminish intestinal tract colonization with VRE and result in decreased VRE infections?

  • Does restriction of vancomycin and anti-anaerobic drugs produce a decreased colonization and infection with VRE?

  • Which is the best methodology to promote and evaluate better practices for environmental cleaning?

  • What are the best treatment options for infections caused by multidrug-resistant and VRE?

What types of infections do enterococci cause?


Enterococci can produce infections at multiple anatomic sites. These include:

  • Bacteremia and vascular catheter-related bloodstream infections (BSIs)

  • Endocarditis

  • Urinary tract infections (UTIs)

  • Abdominal and pelvic infections

  • Skin and soft tissue infections

  • Joint and bone infections

  • CNS infections

  • Pulmonary infections

Over the past three decades there has been a dramatic increase in the rates of enterococcal infections, particular those associated with the healthcare system.

Although some enterococcal infections can be acquired in the community, most of them are nosocomial or healthcare associated infections. Enterococcal infections have a propensity to affect elderly, debilitated or immunocompromised patients whose mucosal barriers and normal flora have been altered by instrumental procedures and/or antibiotic therapy.

Enterococcal infections in humans are mainly caused by E. faecalis and E. faecium and less commonly by other enterococcal species.

Although E. faecalis had been the predominant enterococcal species, about 90% of clinical isolates, in recent years E. faecium has become an important cause of nosocomial and healthcare associated infections, and in many US hospitals it may represent more than 40% of all enterococcal isolates (Table I). Importantly, the increase in E. faecium infections has been associated with high-level antibiotic resistance (to ampicillin, aminoglycosides and vancomycin). The prevalence of vancomycin resistant E. faecium infections in Europe varies widely among countries and is still lower than in the US, but they are increasingly reported (Table II and Table III).

Table I.n

Isolation of Enterococci from Healthcare Associated Infections (HAI) in the United States*

Table II.n

High-level Antibiotic Resistant Enterococci in Patients with Healthcare Associated Infections (HAI) in the United States*

Table III.n

Proportion of High-level Antibiotic Resistance in Enterococcus spp. Bacteraemia in England, Wales, and Northern Ireland (year 2009)

Importantly, molecular studies have suggested that the emergence of E. faecalis and E. faecium as predominant pathogens in hospitals and healthcare settings has resulted from the evolutionary development of specific lineages or clonal complexes, such as E. faecium clonal complex-CC17, with several antibiotic resistance determinants and virulence factors.

Enterococci are often involved in mixed infections, such as intraabdominal suppurative infections, surgical wounds, diabetic foot ulcers, pressure ulcers, and catheter-related BSIs. The pathogenic role of enterococci in mixed infections is difficult to interpret and often these infections can be resolved without effective anti-enterococcal drugs. Enterococcal infections have been associated with the Strongyloides hyperinfection syndrome.

Some descriptions of the main enterococcal infections are given below:

Bacteremia and cathether-related BSIs

Enterococci have become one of the leading causes of nosocomial and healthcare-associated bacteremia. A prospective study using the SCOPE database (from 1995 to 2002) showed that enterococci were responsible for approximately 9% of nosocomial bacteremia cases.

The sources or portal of entry of enterococcal bacteremia may include:

  • Intravascular catheter infections

  • Localized enterococcal infections

  • Intestinal translocation

Intravascular catheter infections

Intravascular catheter infections are a major cause of nosocomial and healthcare associated bacteremia being the most prevalent microorganisms Staphylococci and Enterococci, albeit with lesser extent. Among patients with nosocomial enterococcal bacteremia, an intravascular catheter infection may be the portal of entry in more than 20% of cases. Enterococcal catheter-related bacteremia occur mainly in ICU patients, severely immunocompromised or those with dialysis.

In general, the most important risk factors for, and the prevalence of, catheter-related bacteremia are mainly associated with type of catheter, catheter location and other factors.

Localized enterococcal infections

Bacteremia can be associated with localized enterococcal infections (secondary bacteremia), which is generally associated with worse outcomes than catheter-related bacteremia.

Intestinal translocation

Occasionally, enterococcal bacteremia may not have an apparent portal of entry and when it happens in severely ill or immunocompromised patients often with multiple antimicrobial treatments, a mechanism of intestinal translocation may occur. It has also been demonstrated in experimental models in animals.


Sometimes, the clinical relevance of a positive blood culture for enterococci is difficult to interpret. Most clinicians agree that a confirmed diagnosis of enterococcal bacteremia should be made on the basis of two or more positive blood cultures or one positive blood culture with a positive culture from another sterile site. The clinical significance of a single positive blood culture for enterococci in a febrile patient, without signs of severe sepsis or other suppurative focus of infection, is often unclear, but clinicians should be aware of the presence of a severe immunosuppressive condition, preexisting valvular heart disease or prosthesis. Most patients with enterococcal bacteremia who have not preexisting valvular heart disease or prosthesis will not develop endocarditis.

Enterococci bacteremia is often a polymicrobial infection since enterococci grew together with other microorganisms in blood cultures. Septic shock may occur in the setting of enterococcal bacteremia but it is relatively infrequent and its presence should alert for a polymicrobial infection, particularly in association with a gram-negative bacteria


Mortality associated with enterococcal bacteremia is difficult to assess. Some studies have suggested that bacteremia due to E. faecium may have a worse prognosis than E. faecalis, and it can be partially explained because of an increased resistance to antibiotics in E. faecium. However, it should be noted that the mortality rate in severely ill and immune compromised patients with enterococcal bacteremia may be very high, but it is often unclear whether patients died with or because of the bloodstream infection, and the crude mortality is sometimes confounded by the associated comorbidities. Nevertheless, some studies have suggested that the attributable mortality of enterococcal bloodstream infections is substantial. Patients without severe underlying conditions or endovascular lesions/prostheses are more likely to be able to clear enterococcal bacteremia spontaneously and it becomes an indolent disease.

Enterococci are responsible for 10% to 20% of endocarditis, and in recent series enterococci are the second or third agent causing endocarditis.

Enterococci, particularly E. faecalis and less frequently E. faecium or other enterococcal species, can cause community-acquired, nosocomial-acquired, and healthcare-associated endocarditis. Endocarditis caused by multidrug-resistant enterococci is increasingly reported.

Enterococcal endocarditis occurs more frequently in elderly patients and the source of enterococci is often not found. However, in many cases the portal of entry of enterococci has been a urinary tract infection or a gastrointestinal infection, with subsequent hematogenous spreading and infection of the cardiac valve. Often patients with enterococcal endocarditis have associated a malignant or inflammatory disease and have undergone genitourinary surgery or instrumentation or gastrointestinal instrumentation.

In the case of enterococcal bacteremia the presence of endocarditis should be kept in mind. When enterococcal bacteremia is originated outside the hospital the presence of endocarditis should always be ruled out. However, the presence of endocarditis in patients with nosocomial or healthcare associated enterococcal bacteremia has been very low. Thus, several reports have shown that among patients with a diagnosis of enterococcal bacteremia, the presence of endocarditis varies widely, but it was higher in community-acquired cases (up to 34%) than in hospital-acquired cases (about 1%). However, in recent years there has been an increase of nosocomial and healthcare associated enterococcal endocarditis. The estimated risk of developing endocarditis is higher in E. faecalis bacteremia than in E. faecium bacteremia.

Enterococci usually cause left side endocarditis (mitral or aortic valves) and can affect both native valves – previously damaged heart valve and rarely intact valves – and prosthetic valves. The presentation of enterococcal endocarditis is usually subacute but may be acute, with rapidly progressive valve destruction. Enterococcal endocarditis may display the common signs and symptoms of endocarditis. The most severe complications are heart failure, which may require valve replacement, and embolic events particularly in the brain.

Urinary tract infection

Urinary tract infection (UTI) is the most common infection caused by enterococci, and may present with different clinical syndromes.

Enterococcal UTIs occur rarely in adults without predisposing conditions. Most patients with enterococcal UTIs have some identifiable risk factors.

Although enterococcal UTIs may be community-acquired, most are hospital-acquired or healthcare associated infections. A recent study from the National Healthcare Safety Network shows that enterococci are the third more common organism causing UTIs in patients with urinary catheters.

Enterococcal UTIs may be complicated with bacteremia, but it seems to be relatively uncommon as compared with others pathogens causing UTIs such as Escherichia coli.

In clinical practice it is often difficult to differentiate enterococcal urinary tract colonization from enterococcal UTIs. Some patients (mainly those with urinary catheters) may have only enterococcal urinary tract colonization without symptoms of UTI. Urinary catheters should be removed as soon as possible since it may eradicate enterococci from the urine tract without requiring antibiotic therapy. Mortality due to enterococcal UTIs, in the absence of bacteremia, is very low. However, enterococcal UTIs have been associated with increased length of hospital stay and costs.

Intra-abdominal and pelvic infections

Enterococci have been implicated as an etiologic agent of several intra-abdominal and biliary tract infections as well as in pelvic infections.

There has been a controversy about the role of enterococci in intra-abdominal and pelvic infections since these are frequently mixed infections and enterococci are often associated with other bacteria such as Gram-negative bacilli or anaerobes, and often these patients may recover with surgery and antibiotic regimens that do not include effective anti-enterococcal agents.

However, recent data have shown that in some patients with intra-abdominal infections the isolation of enterococci from abdominal samples is associated with increased rates of postoperative infectious complications, higher number of treatment failures and an increased mortality rate. Thus, although enterococci may not require specific antibiotic coverage in the initial empirical therapy of peritonitis, most clinical authorities believe that those patients who are severely ill or immunocompromised or with factors predisposing to endocarditis as well as those who developed a postoperative peritonitis should receive appropriate treatment for enterococci.

Other infections

These include the following:

  • Skin and soft tissue infections

  • Joint and bone infections

  • CNS infections

  • Pulmonary infections

  • Pediatric infections

What kind of problems does antibiotic resistance in enterococci cause?

Antibiotic resistance in enterocococi

Enterococci may contain (intrinsic) or develop (acquired) resistance to multiple antibiotics, with the most important resistance profiles being to betalactams, aminoglycosides and glycopeptides. Thus, over the past four decades there has been a progressive acquired resistance to several antimicrobials.

Enterococci harbor intrinsic low-level resistance to several antimicrobials. Thus, almost all enterococcal strains are tolerant to betalactams and glycopeptides and resistant to low concentrations of aminoglycosides. Thus, combinations of a cell-wall active compound, a betalactam or glycopeptide, and an aminoglycoside are necessary to achieve consistent bactericidal activity for the treatment of endocarditis and other serious enterococcal infections.

Enterococci have also a remarkable ability to acquire resistance by several mechanisms, such as mutations or acquisition of new resistant genes transferred by plasmids or transposons. Thus, recent progress in genomics has produced new knowledge about distribution and genetic content of mobile genetic elements in enterococci, such as plasmids and transposons. These mobile genetic elements are essential for dissemination and persistence of antimicrobial resistance among enterococci and, even more importantly, to transfer resistant determinants to other bacterial species.

Enterococci are part of the normal bowel flora and it may be crucial for acquiring antibiotic resistance and spreading resistant strains. Thus, the antibiotic use may produce a selective pressure on the colonizing intestinal flora and may favor overgrow and spread of resistant strains and the intra-species or inter-species transmission of resistance genes.

Nowadays, in several hospital or healthcare settings some enterococci, particularly E. faecium, may harbor multiple antibiotic resistances including high-level resistance to ampicillin, aminoglycosides and vancomycin, making the treatment options for serious enterococcal infection a challenge for clinicians.

There are several differences in antibiotic resistance among enterococcal species and some resistances are difficult to detect using standard laboratory methods, and special tests may be required for detecting resistance in clinical isolates.

Beta-lactam resistance

Enterococci exhibit intrinsic resistance to betalactams with increased MICs and loss of their bactericidal activity, also called tolerance.

Enterococcal species may harbor different degrees of betalactam resistance. Thus, E. faecium usually shows a higher intrinsic resistance to betalactams than E. faecalis (e.g., the MICs of ampicillin for E. faecium are about 8 to 32 mcg/mL and for E. faecalis are about 1 to 4 mcg/mL).

Also, betalactam compounds may exhibit different degrees of resistance against enterococci. For instance, the most active betalactams showing the lowest degree of resistance include ampicillin, penicillin G, piperacillin, and imipenem; while those with limited or no activity showing the greatest degree of resistance include aztreonam, ertapenem, cephalosporins, methicillin and ticarcillin. Some new cephalosporins such as ceftobiprole and ceftaroline are active against E. faecalis strains but their activity is lower for most E. faecium strains.

Some enterococci, particularly E. faecalis, have acquired resistance by the ability to produce enzymes such as belactamases, but this resistance mechanism is rarely found and can be easily solved by using a betalactamase inhibitor together with the betalactam agent such as amoxicillin-clavulanic, ampicillin-sulbactam or piperacillin-tazobactam.

A more worrisome therapeutic problem is that some enterococci, particularly E. faecium, may harbor a high-level resistance to ampicillin (i.e., the MICs of ampicillin may be greater than 256 mcg/mL) that appears to be associated with alterations in the PBP5 or transpeptidation mechanisms. Data from the US and UK show that high-level ampicillin/amoxicillin resistance remains relatively low in E. faecalis, but it can reach about 90% in E. faecium (Table II and Table III).

Aminoglycoside resistance

Enterococci exhibit an intrinsic moderate level of resistance to aminoglycosides, with increased gentamicin and streptomycin MICs. The MICs of gentamicin are about 8 to 64 mcg/mL and for streptomycin are about 64 to 512 mcg/mL. The resistance mechanism seems to be a decrease in the permeability of the cell wall that diminishes the entrance of aminoglycosides.

Despite this moderate level of resistance, a synergistic effect, together with a better clinical outcome, can be obtained when adding gentamicin or streptomycin to a regimen with a cell wall active compound (e.g., penicillin, ampicillin or vancomycin). Interestingly, it has been shown that when adding a cell wall active compound that blocks peptidoglycan synthesis markedly increases the cell permeability and the uptake of these aminoglycosides.

In most cases, the synergistic effect cannot be achieved with other aminoglycosides such as tobramycin, kanamycin, and netilmicin since they usually exhibit a high-level resistance because of other resistance mechanisms.

During the last four decades there has been a worldwide dissemination of high-level aminoglycoside-resistant enterococci and there have been several reports showing enterococci with high-level resistance to streptomycin, gentamicin, or both. Then, when using streptomycin or gentamicin in combination with a cell wall active compound (e.g., ampicillin, penicillin or vancomycin), the synergistic effect is not achieved and consequently there is not an improvement of the bactericidal activity necessary for some difficult to treat enterococcal infections (e.g., endocarditis or meningitis). For this reason, the Clinical Laboratory Standards Institute has recommended screening of enterococci for high-level resistance to streptomycin and gentamicin.

According to the European Centre for Disease Prevention and Control 2009 report (, the proportion of high-level aminoglycoside resistance in E. faecalis was above 50% in three countries (Greece, Cyprus and Hungary) and between 30% and 50% in the majority of other European countries. Among enterococcal bacteremia cases from the UK in 2009 the proportion of high-level gentamicin resistance was similar and was higher for E. faecium than for E. faecalis (Table III). The prevalence of enterococcal strains with high-level resistance to aminoglycosides may experience large variations over time due to outbreaks.

The treatment of endocarditis due to E. faecalis with high-level resistance to aminoglycosides has become a worrisome problem. However, it has been suggested that the combination of ceftriaxone or cefotaxime with ampicillin may be more effective than ampicillin alone, and this synergistic combination may be an alternative therapy for patients with aminoglycoside resistant E. faecalis endocarditis. However, the synergistic effect with these combination regimens was not observed with E. faecium

Glycopeptide resistance

There are some enterococcal species such as E. gallinarum and E. casseliflavus that harbor an intrinsic low-level resistance to vancomycin (MICs 8 to 16 mcg/mL). But the most important problem has been that Enterococci have developed low-level and high-level resistance to glycopeptides, cell wall acting compounds, such as vancomycin and teicoplanin, which has been associated with van gen clusters.

The Clinical and Laboratory Standards Institute (CLSI) has reported the following vancomycin breakpoints:

  • Susceptible (MIC ≤4 mcg/mL)

  • Intermediate (MIC 8 to 16 mcg/mL) and

  • Resistant (MIC ≥32 mcg/mL).

Importantly, sometimes there are difficulties in detecting vancomycin resistance in enterococci when using standard laboratory tests, that may require additional methods. Vancomycin therapy should not be recommended for patients with enterococcal isolates showing intermediate or high level vancomycin resistance.

High level resistance to vancomycin is an increasingly reported clinical and therapeutic problem, because it often appears in enterococcal strains, particularly E. faecium, that also harbor high-level resistance to ampicillin.

The increased vancomycin resistance in enterococci in the US has been associated with the increasing use of vancomycin for treating other infections such as methicillin-resistant Staphylococcus aureus (MRSA), methicillin-resistant coagulase negative staphylococci, and Clostridium difficile.

High-level vancomycin resistance in enterococci is usually encoded by resistant gene clusters such as vanA, vanB, and vanD, while low-level vancomycin resistance is usually encoded by gene clusters such as vanC, vanE, vanG, vanL, and vanN (Table IV). In clinical practice, high-level vancomycin resistance is most commonly associated with vanA and generate cross-resistance to teicoplanin. The origins of van gen clusters are not fully understood but homologs of van genes have also been found in the biopesticide Bacillus popilliae and bacteria colonizing the intestinal tract such as Clostridium inoculums which suggest that other bacteria could be a potential source of van gen homologs.

Table IV.n

Proportion of high-level antibiotic resistance in Enterococcus spp. bacteraemia in England, Wales, and Northern Ireland (year 2009)

Some reports have demonstrated the intraspecies and interspecies transmission of vancomycin resistance and the vanA cluster can disseminate from enterococci to other prevalent nosocomial bacterial species such as methicillin-resistant Staphylococcus aureus (MRSA) and produce a great problem in the hospital setting.

According to the European Centre for Disease Prevention and Control 2009 report ( regarding vancomycin resistance in E. faecium, three European countries reported resistance proportions above 25% (Ireland, Greece and Luxembourg) and five countries reported resistance proportions between 10% and 25% (UK, Portugal, Lithuania, Latvia and Cyprus), while the majority of countries reported resistance proportions between < 1% and 10%.

Other antibiotic resistances

Different degrees of resistance in enterococci that can be intrinsically or acquired are frequently found among antibiotics such as trimethoprim-sulfamethoxazole, macrolides, tetracyclines or fluoroquinolones which are not usually included in the armamentarium for treating enterococcal infections. In several US hospitals the prevalence of vancomycin resistant E. faecium is very high (Table II), while in Europe it varies widely among countries but, in general, has experienced an increase in the years 2000s.

Newer antibiotics such as linezolid, daptomycin, quinupristin-dalfopristin, tigecycline and lypoglycopeptides usually show good activity against multidrug-resistant enterococci; however, resistance to these agents has already been reported.

  • Linezolid resistance

  • Daptomycin resistance

  • Quinupristin-dalfopristin resistance

  • Tigecycline resistance

  • Lipoglycopeptides resistance

What is the epidemiology of vancomycin resistant enterococci?

Epidemiology of vancomycin resistant enterococci

Enterococci have become resistant to multiple antimicrobial agents (e.g., betalactams, aminoglycosides, glycopeptides) and as resistance increases, the control of emergence and spread of resistant enterococci becomes more imperative.

In recent years, control of vancomycin resistant enterococci (VRE) in the healthcare setting has become a real challenge for epidemiologists and clinicians. Most of infection control measures for preventing VRE are also applicable, in large, to other drug-resistant enterococci and other resistant bacteria.

Vancomycin resistant enterococci (VRE) can colonize the gastrointestinal tract, particularly the large bowel, and is an important cause of nosocomial and healthcare-associated infections. Isolation of VRE in person without prior hospitalization or without contact with the healthcare system is very rare.

Large differences exist among enterococcal species regarding resistance to vancomycin. Thus, the majority of VRE isolates are E. faecium and less frequently E. faecalis; for example, data from the NHSN (2006-2007) showed that 80% of E. faecium and 6.9% of E. faecalis were vancomycin resistant (see Table II).

VRE bowel colonization can contaminate the skin due to fecal shedding. Patients colonized with VRE serve as a reservoir and can transmit the strains to other patients through the healthcare workers and contaminated materials. Colonization with VRE usually anticipates infection, but not all colonized patients will become infected.

Infections caused by VRE have become a difficult to treat infection in patients admitted to hospitals, long-term care facilities, or in other healthcare settings.

Interestingly, several reports have demonstrated clear differences in the epidemiology of VRE between Europe and the U.S. Thus, VRE infections in humans were initially reported in Europe in the late 1980s and were associated to the widely use of avoparcin, a glycopeptide compound, as a food additive for growth promotion in animals (VRE could be recovered from the bowel flora of many animals such as chicken, fowl and pigs). Thus, in Europe there was an evident link between an animal source of VRE and subsequent transmission to humans.

Later on, VRE infections were detected in the U.S. hospitals, where these infections were associated with an increased use of vancomycin in hospitalized patients. However, in the U.S., where avoparcin was not used for growth promoting in animals, there was no clear evidence of an animal source of VRE as occurred in Europe. Recently, a report from Michigan showed an isolation of VRE from pigs.

In humans, some enterococcal species such as E. casseliflavus and E. flavescens harbor intrinsic low-level vancomycin resistance may colonize the intestinal tract, but enterococci with high-level vancomycin resistance are not usually seen as colonizers. Then, in humans the bowel colonization with high-level vancomycin resistant enterococci having van A or van B gene cluster may result from an animal source or by horizontal transfer within the hospital or other healthcare settings.

Several reports have shown that VRE infections have been detected worldwide but the prevalence of these infections varies widely among countries. Of note, in the last two decades (1990s and 2000s) the rates of VRE infections in the U.S. have steadily increased, while in Europe these rates have persisted relatively lower than in the U.S. However, in recent years VRE are increasingly reported in some European countries (e.g. U.K., Portugal, Greece) while in others their prevalence is persistently relatively low.

VRE have produced multiple outbreaks in hospitalized patients, particularly in severely ill or immunocompromised patients admitted to ICUs as well as in surgical wards and medical wards. In more recent years, VRE have become endemic in many hospitals and chronic care facilities.

Analyses with molecular techniques such as PFGF (pulsed-field gel electrophoresis) have been useful to clarify the epidemiology of VRE in the hospital setting. Thus, several reports have shown that a single VRE clone can spread within a hospital unit and produce outbreaks. On the other hand, however, VRE strains can also transfer resistance horizontally to unrelated enterococcal strains and then many different VRE clones (different PFGF profiles) can be found in a single hospital and, in these circumstances, VRE may become endemic.

The epidemiology of VRE is not fully understood, but the emergence and spread of VRE may be a consequence of a complex interaction among several factors such as:

  • The use of antibiotics in animals and human beings.

  • The persistence of VRE in colonized animals and humans as well as in environmental and dietary reservoirs.

  • The potential for the rapid spread within hospitals and healthcare facilities where debilitated and immune compromised patients are admitted.

Risk factors for vancomycin resistant enterococci

It is well known that patients with VRE colonization in the intestinal tract sever as a reservoir and it is the initial step for spreading VRE in a healthcare setting and cause VRE infections (see Table V).

Table V.n

Major risk factors for vancomycin resistant enterococci

VRE bowel colonization is usually detected by the use of rectal or perirectal swab cultures or stool cultures. The sensitivity of rectal swab varies widely depending on the VRE density in stool. Patients with high stool densities, prior antibiotics and associated skin colonization are those with higher probability of having positive rectal swab cultures for VRE.

The lack of identification of carriers because of false-negative rectal swab cultures, which may avoid the implementation of contact precautions, may increase transmission of VRE. Transmission of VRE from colonized patients to non-colonized patients can occur directly by contaminated hands of healthcare workers or indirectly by contaminated environmental surfaces. It has been demonstrated that VRE can survive for several days in different environmental surfaces (e.g., bedrails, countertops) and medical devices (e.g., stethoscopes, thermometers).

Multiple reports have evaluated the risk factors associated with VRE and there are several identifiable risk factors for infection and/or colonization with VRE, such as:

Patient characteristics and site of care

Several characteristics of patients have been associated with high risk of VRE such as the presence of serious underlying diseases (e.g., malignant disease and neutropenia, organ transplant recipients, chronic renal failure) and the use of invasive devices (e.g., intravascular catheters or urinary catheters).

In addition, patients admitted to ICUs and those with a prolonged hospital stay are at high risk for VRE. Some reports have also demonstrated that patients admitted to long-term care facilities are at high risk of VRE, particularly if the colonized pressure is high in those facilities. Often these patients have debilitating and chronic underlying conditions, suffer from decubitus ulcer, and receive multiple antibiotic treatments. Patients from nursing homes carrying VRE often introduce the strains to acute care facilities.

Prior antibiotics

Antibiotics may modify the normal bowel flora and predispose to colonization with resistant organisms. Thus, the use of antibiotics seems to be an important risk factor for VRE and multiple studies have demonstrated an association between prior antibiotic therapy and colonization or infection with VRE. Thus, patients with VRE had often prior antibiotic therapy with vancomycin, cephalosporins, anti-anaerobic drugs or quinolones, often with prolonged courses of treatment. The antibiotic selection pressure, particularly with anti-anaerobic drugs, may change the normal balance of the bowel flora and increase density of colonization with VRE.

Colonization pressure

The daily point prevalence of VRE colonized patients in a specific hospital unit is a crucial risk factor for acquisition of VRE. Thus, the risk for hospitalized patients to be colonized with VRE is strongly correlated with the number of VRE carriers and/or infected patients admitted in the hospital unit.

Environmental contamination

It has been demonstrated that exposure of hospitalized patients to contaminated surfaces and medical equipment is associated with VRE colonization and outbreaks of VRE infections.

The inappropriate use of hand washing and gloves by healthcare workers may transfer VRE from contaminated surfaces to uncontaminated surfaces and to uncontaminated patients.

An appropriate compliance by the housekeeping staff of the cleaning protocols to avoid or diminish environmental contamination with VRE should be mandatory

Control of VRE

Multiple experiences and reports have confirmed the beneficial effect of several infection control measures for preventing colonization and infection with VRE (see Table IV). One important step in interrupting transmission of VRE is early identification of colonized and/or infected patients. Once VRE have disseminated in a hospital unit, their eradication may become a very difficult issue.

For an effective control of VRE several steps are mandatory:

  • First, the microbiology laboratory must play an active role in the control of VRE by classifying the enterococci at the species level and determining antimicrobial susceptibilities on clinical isolates using accurate methods.

  • Secondly, control of infection with VRE require of different approaches.

  • Thirdly, several strategies for prevention of transmission of VRE must be implemented.

Strategies for prevention of transmission of VRE include the following five items:

1. Hand hygiene, contact precautions, and source control

Hand hygiene is considered the most important measure of preventing spread of VRE from patient to patient through the hands of healthcare workers. The two recognized techniques for hand hygiene are hand washing with soap and water and hand rubbing with alcohol-based hand-rub formulations. Proper use of hand hygiene is considered a critical issue for the prevention of VRE, and it should be performed immediately before and after touching a patient or touching objects located in the patient’s room. Several factors may influence the efficacy of hand hygiene and these include a proper duration of hand washing (it should take > 20 seconds) and use of soap.

Contact/barrier precautions can reduce the spread of VRE. Thus, transmission of VRE may decrease when healthcare workers wear gloves properly and gown when taking care of their patients, putting them on when entering a patient room, and removing them prior to exiting. It has been demonstrated that the use of gloves and gown is more efficacious than the use of gloves alone. It is important to clarify precisely when and how patients with VRE should be placed on contact precautions. Each institution should have available routes of electronic information of contact/barrier precautions requirements and initiation of isolation.

Education targeted to healthcare workers, cleaning and food service staff and visitors may help correct nonadherent practices to contact/barriers precautions and isolation measures. Finally, regular monitoring of contact/barrier precautions and revising the design of planned interventions are important to ascertain whether the recommendations are being followed and have any impact. Also the leaders and/or healthcare workers and staff should have a regular feedback of the process and appropriate recommendations for changes in order to increase behavioral adherence.

Source control, defined as a regular bathing of patients with antiseptic agents such as chlorhexidine, can reduce the burden of skin colonization by VRE and MRSA, and is an effective measure for preventing bloodstream infections.

When can a colonized patient with VRE be removed from contact precautions?

It has been recommended that for removing a patient from contact precautions he/she should have at least three negative rectal/perirectal or stool cultures obtained at weekly intervals. Importantly, however, these patients may persist with VRE colonization for more than one year, and rectal/perirectal or stools cultures may become positive after a new course of antibiotic therapy.

2. Cohorting of patients and/or healthcare workers

In the setting of colonization with multidrug-resistant organisms including VRE, cohorting of patients and/or cohorting of healthcare workers (e.g., nursing staff that take care for colonized or infected patients should not care for other patients) may diminish the transmission of VRE. In addition, several experiences have shown that using private rooms or closing units during outbreaks can help to reduce transmission of multidrug-resistant organisms.

Certain items of medical equipment such as thermometers, blood pressure cuffs and stethoscopes should be confined to the isolation room and not used for other patients.

Roommates of patients infected or colonized with VRE should have rectal/perirectal or stool cultures obtained.

Patients who had been colonized or infected with VRE and are readmitted to the hospital should be placed in isolation until colonization can be ruled out (e.g., two negative rectal/perirectal/stool cultures obtained at least 48 hours apart).

3. Surveillance studies for detecting colonization

Active surveillance cultures facilitate identification of patients with VRE carriage to be placed on contact precautions to minimize VRE spread. The most common specimens obtained to detect VRE carriage are rectal/perirectal swabs and stool samples.

Several studies have shown that performance of active surveillance cultures, on admission and periodically during hospitalization, for VRE carriage and further implementation of other control measures in patients at high risk can reduce transmission of VRE. It may be particularly important in patients admitted to ICUs and hematology/oncology wards or during outbreaks of infections caused by VRE.

What patients need active surveillance cultures?

It is well known that patients colonized with VRE, particularly those severely ill or immunocompromised, are at higher risk for developing VRE infections.

Active surveillance cultures of hospitalized patients for VRE carriage can be an effective strategy to implement rational preventive measures and should be carried out in patients at high risk. However, legislation has been introduced in some states in the U.S. where all hospitalized patients (not only patients at high risk) need to have performed surveillance cultures for MRSA and/or VRE. However, different professional organizations such as the Society for Healthcare Epidemiology of America (SHEA) and the Association of Professionals in Infection Control and Epidemiology (APIC) have expressed some concerns regarding this legislation. Moreover, a recent study has prospectively evaluated the culture-based active surveillance for MRSA and VRE and the expanded use of barrier precautions in 10 ICUs, as compared with existing practice in 8 ICUs. And, the conclusion was that the intervention was not effective in reducing the transmission of MRSA and VRE, although the use of barrier precautions was not optimal.

It is important to know that patients who had an infection or were colonized with VRE may remain culture-positive for more than 1 year and therefore active surveillance cultures are not needed for most of these patients.

Several decolonization strategies have been used to eradicate VRE carriage. However, current data show that intestinal decolonization with nonabsorbable oral antibiotics has not proved to be consistently effective and most authorities are not currently recommended it.

4. Prudent use of antibiotics

Most authorities consider that a prudent use of antibiotics is a fundamental strategy to reduce problems with antimicrobial resistance in the healthcare setting.

Thus, antibiotics must be administered prudently, with appropriate doses and duration of treatment. Inappropriate and excessive use of antibiotics can lead to selection of resistant organisms. For example, the risk of MRSA colonization has been correlated with a long duration of prior antibiotic therapy and certain types of antibiotics such as quinolones.

Although the relevance of antibiotic restriction in controlling VRE has not been clearly established, most authorities agree that antibiotic restriction, particularly vancomycin, cephalosporins, and anti-anaerobic drugs, should be considered in the setting of a nosocomial outbreak of VRE. For example, vancomycin should be avoided for routine prophylaxis unless high rates of MRSA exist. Also, vancomycin should be avoided for the treatment of coagulase-negative staphylococci bacteremia growing in a single blood culture if contamination is likely.

5. Environmental cleaning

In many circumstances transmission of VRE is related to contamination of near-patient surfaces and medical equipment. Often the evaluation of environmental cleaning is difficult to ascertain and some reports have confirmed that most near patient surfaces are not being cleaned in accordance with existing hospital policies.

Housekeeping staff should be instructed to clean properly the patient’s room, particularly the high touch surfaces and equipments, on a daily basis. After the patient is discharged or transferred, the room should be accurately cleaned and disinfected.

The cleaning process could be improved with the use of new techniques such as saturated steam vapor disinfectant systems.

The CDC initiative clearly emphasizes the need for improving the environmental cleaning and encourages hospitals to implement programs for optimizing it (basic or Level I program and Level II program). The CDC initiative claims to dedicate resources for evaluating environmental hygiene by means of implementing objective monitoring methods (e.g., direct practice observation, swab cultures, agar slide cultures, fluorescence markers, ATP bioluminesence). However, the local hospital or healthcare institution should consider the advantages and limitations of these monitoring approaches (

What are the treatment options for enterococcal infections?

Treatment of enterococcal infections remains a difficult issue. Most currently available data are derived from uncontrolled studies. Several considerations should be taken into account and these may include:

  • Enterococci may harbor intrinsic antimicrobial resistance and more importantly, they have developed an escalating process of acquiring new resistant determinants.

  • Enterococcal infections often occur in a debilitated host.

  • Enterococci are frequently cultured from mixed infections.

  • There are some controversies related to using monotherapy versus combination therapy in enterococcal infections.

  • Treatment options for cases with high-level resistance for both ampicillin (non-betalactamase producing strains) and vancomycin.

Table VII summarizes the antimicrobial agents for enterococci. Briefly, some specific treatment options for the most common enterococcal infections are summarized below:

Table VI.n

Major infection control measures for the prevention of vancomycin-resistant enterococci

Table VII.n

Antimicrobial Agents for the Treatment of Enterococcal Infections

Bacteremia and catheter-related BSIs

Treatment of enterococcal bacteremia may include intravenous ampicillin as the treatment of choice and vancomycin in cases with ampicillin resistance; linezolid or daptomycin can be used in cases resistant to ampicillin and vancomycin. Doubts exist as to whether it should be monotherapy or combination therapy, which may include ampicillin or vancomycin plus gentamicin or streptomycin, in order to obtain a synergistic effect. Most authorities favor monotherapy for most cases of enterococcal bacteremia and combination therapy in severe sepsis or critically ill patients or those with preexisting valvular disease. In general, antibiotic therapy should be given for 7 to 14 days, although the optimal duration of treatment has not been established.

In the case of catheter-related BSIs, catheter removal alone may cure the infection, and most of these patients resolve the infection after 7 days of antibiotic therapy. No randomized trials have evaluated the potential benefit of combination therapy versus monotherapy or the optimal duration of therapy. However, most clinicians believe that many patients with enterococcal catheter-related BSIs can be cured with monotherapy and in cases of severe sepsis or critically-ill patients or those with risk factors for endocarditis or in whom intravascular catheter remains in situ a combination therapy and/or a prolonged duration of treatment should be considered.


The treatment of choice for enterococcal endocarditis is ampicillin or penicillin G plus gentamicin. The usual duration of treatment is 4 to 6 weeks; however, to avoid nephrotoxity and ototoxicity, a shorter course of aminoglycoside (2 weeks) may be recommended in some cases, e.g., small vegetarians or patients with native endocarditis without prosthetic valves. If strains are producing beta-lactamase, the use of ampicillin-sulbactam plus gentamicin or vancomycin plus gentamicin is usually recommended. In the setting of high-level penicillin resistance, the use of vancomycin plus gentamicin is recommended; if high-level gentamicin resistance is detected, streptomycin may be the alternative.

In the setting of aminoglycoside resistant E. faecalis, other combinations such as ampicillin plus imipenem or ampicillin plus ceftriaxone or ceftotaxime have been recommended. For multi-drug resistant E. faecium, linezolid or quinupristin-dalfopristin may be used. Daptomycin is generally not recommended for enterococcal endocarditis, although high-dose daptomycin combined with other agents such as gentamicin, rifampin, or tigecycline have cured some patients with vancomycin resistant enterococcal endocarditis. Importantly, in cases with multiple resistances the treatment success is usually lower and the duration of treatment should be prolonged at least of 8 weeks.

Urinary tract infections (UTIs)

Oral therapy for uncomplicated enterococcal UTIs may include amoxicillin, nitrofurantoin, or fosfomycin; the experience with linezolid or fluoroquinolones is limited. For complicated UTIs, intravenous ampicillin is considered the drug of choice; alternatives may include vancomycin for susceptible cases or linezolid for cases resistant to ampicillin and vancomycin.

Intra-abdominal infections

It has been suggested that empiric antibiotic therapy for most community-acquired intra-abdominal infections or peritonitis does not need to cover enterococci. However, enterococci should be covered in selected patients with peritonitis such as those with prior antibiotics, immunocompromised host, those with valvular disease or prosthesis, as well as those with postoperative peritonitis. Antibiotics with a potential activity against enterococci, which must be confirmed with susceptibility studies, may include ampicillin, piperacillin-tazobactam, imipenem, or vancomycin. The coverage of VRE and/or multidrug resistant enterococci should be considered in endemic or epidemic settings and may require new alternative agents.


Treatment of enterococcal meningitis is a difficult issue. Most clinicians agree that a combination of drugs to achieve synergistic therapy with systemic antibiotics (i.e., ampicillin or penicillin or vancomycin plus gentamicin or streptomycin) should be given for most cases of enterococcal meningitis. Some patients may require an intraventricular therapy (e.g., vancomycin or gentamicin). Experience with multi-resistant E. faecium meningitis is very limited and requires alternative agents given alone or in combinations, such as quinupristin-dalfopristin and rifampin. Other agents such as daptomycin and tigecycline have poor CNS penetration.

What national and international guidelines exist related to Gram positive bacteria – Enterococcus?

Guidelines to prevent transmission of VRE

There is a debate on optimal infection control strategies for preventing multidrug resistant organisms and VRE. In addition, most studies have been carried out in acute care institutions, and with lesser extent in non-acute care institutions or chronic care facilities.

There have been several organizations that reported guideline recommendations to prevent transmission of multidrug resistant organisms including VRE. These evidence-based guidelines include The Society for Healthcare Epidemiology of America (SHEA), the Hospital Infection Society and Infection Control Nurses Association in UK, and the Hospital Infection Control Practices Advisory Committee (HICPAC) of the CDC.

In brief, the SHEA guidelines include several recommendations based on the level of scientific evidence for each infection control measures that should be implemented for preventing multidrug resistant strains of Staphylococcus aureus and Enterococcus.

The U.K. guidelines also provide recommendations for the control of glycopeptides-resistant enterococci and categorized the preventive measures according to the level of scientific evidence.

The HICPAC guidelines present a two-tiered approach for control of multidrug resistant organisms including VRE. Tier-1 includes general recommendations for routine prevention and control of multidrug resistant organisms, and Tier-2 includes recommendations for intensified multidrug resistant organisms control efforts in special situations such as an outbreak or high incidence rates. Tier-1 and Tier-2 include seven categories of intervention.

  • Administrative measures/adherence monitoring

  • Multidrug resistant organisms education

  • Judicious antimicrobial use

  • Surveillance

  • Infection control precautions to prevent transmission

  • Environmental measures

  • Decolonization

All three guidelines mostly agree regarding the main infection control strategies for prevention colonization/infection with multidrug resistant organisms and VRE. However, these guidelines differ regarding the use of active surveillance cultures for detecting colonization with VRE in patients at high risk. The UK guideline did not particularly mention active surveillance cultures as a recommended practice among the infection control measures for VRE. The SHEA guideline recommends the use of surveillance cultures in patients at high risk. The HICPAC guideline includes two-tiered set of recommendations.

All three guidelines agree that no recommendations can be made for decolonization of patients who carry VRE and the use of nonabsorbable oral antibiotics has been generally disappointing.

The guidelines emphasize that compliance with hand hygiene practices and contact/barrier precautions are critical for preventing the spread of multidrug resistant organisms and VRE, but implementation is a challenge at many healthcare institutions. It is clear that the infection control program should be a dynamic process that requires a systematic approach and have precise measures for entering or removing a patient from contact/barrier precautions to promote adherent practices.

Also, the infection control program should identify nonadherent practices. It is important to emphasize that despite publication of detailed recommendations and guidelines, compliance remains suboptimal in many institutions. For example, a report from three New York institutions showed that patient care staff had an adherence rates on room entry and exit of 22.4% and 59.0% for hand hygiene, 71.6% and 72.5% for gloves, and 71.0% and 83.9% for gowns. Another multicenter study, which includes several ICUs from the US, showed that after an intervention (using surveillance cultures and reinforcing barriers precautions) health care providers used gloves, gowns and hand hygiene less frequently than required.

In summary, the hospitals and healthcare institutions need to reinforce the major infection control strategies such as hand hygiene and contact/barrier precautions, use antibiotics prudently, and proper environmental cleaning. Compliance with the current evidence-based guidelines is mandatory in order to reduce colonization and infection with VRE.

What other consensus group statements exist and what do key leaders advise?

See above.

Enterococci and enterococcal infections

Murray, BE. “The life and times of the Enterococcus”. Clin Microbiol Rev. vol. 3. 1990 Jan. pp. 46-65.

Fisher, K, Phillips, C. “The ecology, epidemiology and virulence of Enterococcus”. Microbiology. vol. 155. 2009 Jun. pp. 1749-57.

Tan, CK, Lai, CC, Wang, JY. “Bacteremia caused by non-faecalis and non-faecium enterococcus species at a medical center in Taiwan, 2000 to 2008”. JOURNAL OF INFECTION. vol. 61. 2010. pp. 34-43.

Shirano, M, Takakura, S, Yamamoto, M, Matsumura, Y, Matsushima, A, Nagao, M, Fujihara, N, Saito, T, Ito, Y, Iinuma, Y, Shimizu, T, Fujita, N, Ichiyama, S. “Regional spread of vanA- or vanB-positive Enterococcus gallinarum in hospitals and long-term care facilities in Kyoto prefecture, Japan”. Epidemiol Infect. vol. 139. 2011 Mar. pp. 430-6.

Wade, JJ. “Enterococcus faecium in hospitals”. Eur J Clin Microbiol Infect Dis. vol. 16. 1997 Feb. pp. 113-9.

McBride, SJ, Upton, A, Roberts, SA. “Clinical characteristics and outcomes of patients with vancomycin-susceptible Enterococcus faecalis and Enterococcus faecium bacteraemia–a five-year retrospective review”. Eur J Clin Microbiol Infect Dis. vol. 29. 2010 Jan. pp. 107-14.

Butler, AM, Olsen, MA, Merz, LR, Guth, RM, Woeltje, KF, Camins, BC, Fraser, VJ. “Attributable costs of enterococcal bloodstream infections in a nonsurgical hospital cohort”. Infect Control Hosp Epidemiol. vol. 31. 2010 Jan. pp. 28-35.

Suppli, M, Aabenhus, R, Harboe, ZB, Andersen, LP, Tvede, M, Jensen, JU. “Mortality in enterococcal bloodstream infections increases with inappropriate antimicrobial therapy”. Clin Microbiol Infect. 2010 Oct 14.

Huycke, MM, Sahm, DF, Gilmore, MS. “Multiple-drug resistant enterococci: the nature of the problem and an agenda for the future”. Emerg Infect Dis. vol. 4. 1998 Apr-Jun. pp. 239-49.

Tyrrell, GJ, Bethune, RN, Willey, B, Low, DE. “Species identification of enterococci via intergenic ribosomal PCR”. J Clin Microbiol. vol. 35. 1997. pp. 1054-60.

Depardieu, F, Perichon, B, Courvalin, P. “Detection of the van alphabet and identification of enterococci and staphylococci at the species level by multiplex PCR”. J Clin Microbiol. vol. 42. 2004. pp. 5857-60.

van Schaik, W, Willems, RJL. “Genome-based insights into the evolution of enterococci”. Clin Microbiol Infect. vol. 16. 2010. pp. 527-532.

Sava, IG, Heikens, E, Huebner, J. “Pathogenesis and immunity in enterococcal infections”. Clin Microbiol Infect. vol. 16. 2010. pp. 533-540.

Choudhury, T, Singh, KV, Sillanpää, J, Nallapareddy, SR, Murray, BE. “Importance of two Enterococcus faecium loci encoding Gls-like proteins for in vitro bile salts stress response and virulence”. J Infect Dis. vol. 203. 2011 Apr 15. pp. 1147-54.

Brede, DA, Snipen, LG, Ussery, DW, Nederbragt, AJ, Nes, IF. “Complete Genome Sequence of the Commensal Enterococcus faecalis 62, Isolated from a Healthy Norwegian Infant”. J Bacteriol. vol. 193. 2011 May. pp. 2377-8.

Laverde Gomez, JA, Hendrickx, AP, Willems, RJ, Top, J, Sava, I, Huebner, J, Witte, W, Werner, G. “Intra- and Interspecies Genomic Transfer of the Enterococcus faecalis Pathogenicity Island”. PLoS One. vol. 6. 2011. pp. e16720

Morrison, AJ, Wenzel, RP. “Nosocomial urinary infections due to enterococci: ten years’ experience at a university hospital”. Arch Intern Med. vol. 146. 1986. pp. 1549-51.

Maki, DG, Agger, WA. “Enterococcal bacteremia: clinical features, the risk of endocarditis, and management”. Medicine. vol. 67. 1988. pp. 248-69.

Pallares, R, Pujol, M, Peña, C, Ariza, J, Martin, R, Gudiol, F. “Cephalosporins as risk factor for nosocomial Enterococcus faecalis bacteremia”. A matched case-control study. Arch Intern Med. vol. 153. 1993. pp. 1581-6.

Zervos, MJ, Bacon, AE, Patterson, JE. “Enterococcal superinfection in patients treated with ciprofloxacin”. J Antimicrob Chemother. vol. 21. 1988. pp. 113-15.

Ariza, J, Gudiol, F, Dolz, C, Xiol, J, Liñares, J, Pallares, R. “Evaluation of aztreonam in the treatment of spontaneous bacterial peritonitis in patients with cirrhosis”. Hepatology. vol. 6. 1986. pp. 906-10.

Top, J, Willems, R, Bonten, M. “Emergence of CC17 Enterococcus faecium: from commensal to hospital-adapted pathogen”. FEMS Immunol Med Microbiol. vol. 52. 2008 Apr. pp. 297-308.

Willems, RJ, Top, J, van Santen, M, Robinson, DA, Coque, TM, Baquero, F, Grundmann, H, Bonten, MJ. “Global spread of vancomycin-resistant Enterococcus faecium from distinct nosocomial genetic complex”. Emerg Infect Dis. vol. 11. 2005 Jun. pp. 821-8.

Galloway-Peña, JR, Nallapareddy, SR, Arias, CA, Eliopoulos, GM, Murray, BE. “Analysis of clonality and antibiotic resistance among early clinical isolates of Enterococcus faecium in the United States”. J Infect Dis. vol. 200. 2009 Nov 15. pp. 1566-73.

McBride, SM, Fischetti, VA, Leblanc, DJ, Moellering, RC, Gilmore, MS. “Genetic diversity among Enterococcus faecalis”. PLoS One. vol. 2. 2007 Jul 4. -e582.

Bamias, G, Toskas, A, Psychogiou, M, Delladetsima, I, Siakavellas, SI, Dimarogona, K, Daikos, GL. “Strongyloides hyperinfection syndrome presenting as enterococcal meningitis in a low-endemicity area”. Virulence. vol. 1. 2010 Sep-Oct. pp. 468-70.

Wisplinghoff, H, Bischoff, T, Tallent, SM, Seifert, H, Wenzel, RP, Edmond, MB. “Nosocomial bloodstream infections in US hospitals: analysis of 24,179 cases from a prospective nationwide surveillance study”. Clin Infect Dis. vol. 39. 2004 Aug 1. pp. 309-17.

Sandoe, JA, Witherden, IR, Au-Yeung, HK, Kite, P, Kerr, KG, Wilcox, MH. “Enterococcal intravascular catheter-related bloodstream infection: management and outcome of 61 consecutive cases”. J Antimicrob Chemother. vol. 50. 2002 Oct. pp. 577-82.

Marr, KA, Sexton, DJ, Conlon, PJ. “Catheter-related bacteremia and outcome of attempted catheter salvage in patients undergoing hemodialysis”. Ann Intern Med. vol. 127. 1997. pp. 275

Allon, M. “Dialysis catheter-related bacteremia: treatment and prophylaxis”. Am J Kidney Dis. vol. 44. 2004. pp. 779-91.

Mitchell, D, Krishnasami, Z, Allon, M. “Catheter-related bacteraemia in haemodialysis patients with HIV infection”. Nephrol Dial Transplant. vol. 21. 2006. pp. 3185-86.

Mermel, LA, Allon, M, Bouza, E. “Clinical practice guidelines for the diagnosis and management of intravascular catheter-related infection: 2009 Update by the Infectious Diseases Society of America”. Clin Infect Dis. vol. 49. 2009. pp. 1

Lorente, L, Jiménez, A, Santana, M. “Microorganisms responsible for intravascular catheter-related bloodstream infection according to the catheter site”. Crit Care Med. vol. 35. 2007. pp. 2424-7.

Patterson, JE, Sweeney, AH, Simms, M. “An analysis of 110 serious enterococcal infections. Epidemiology, antibiotic susceptibility, and outcome”. Medicine (Baltimore). vol. 74. 1995. pp. 191-200.

Graninger, W, Ragette, R. “Nosocomial bacteremia due to Enterococcus faecalis without endocarditis”. Clin Infect Dis. vol. 15. 1992. pp. 49-57.

Wells, CL, Jechorek, RP, Maddaus, MA, Simmons, RL. “Effects of clindamycin and metronidazole on the intestinal colonization and translocation of enterococci in mice”. Antimicrob Agents Chemother. vol. 32. 1988 Dec. pp. 1769-75.

Wells, CL, Jechorek, RP, Erlandsen, SL. “Evidence for the translocation of Enterococcus faecalis across the mouse intestinal tract”. J Infect Dis. vol. 162. 1990 Jul. pp. 82-90.

Fernández-Guerrero, ML, Herrero, L, Bellver, M. “Nosocomial enterococcal endocarditis: a serious hazard for hospitalized patients with enterococcal bacteraemia”. J Intern Med. vol. 252. 2002. pp. 510

Vergis, EN, Hayden, MK, Chow, JW. “Determinants of vancomycin resistance and mortality rates in enterococcal bacteremia. A prospective multicenter study”. Ann Intern Med. vol. 135. 2001. pp. 484-92.

Edmond, MB, Wallace, SE, McClish, DK. “Nosocomial bloodstream infections in United States hospitals: a three-year analysis”. Clin Infect Dis. vol. 29. 1999. pp. 239-44.

Anderson, DJ, Murdoch, DR, Sexton, DJ. “Risk factors for infective endocarditis in patients with enterococcal bacteremia: a case-control study”. Infection. vol. 32. 2004. pp. 72-77.

Weinstein, MP, Towns, ML, Quartey, SM. “The clinical significance of positive blood cultures in the 1990s: a prospective comprehensive evaluation of the microbiology, epidemiology, and outcome of bacteremia and fungemia in adults”. Clin Infect Dis. vol. 24. 1997. pp. 584-602.

Garrison, RN, Fry, DE, Berberich, S. “Enterococcal bacteremia: clinical implications and determinants of death”. Ann Surg. vol. 196. 1982. pp. 43-47.

Ghanem, G, Hachem, R, Jiang, Y. “Outcomes for and risk factors associated with vancomycin-resistant Enterococcus faecalis and vancomycin-resistant Enterococcus faecium bacteremia in cancer patients”. Infect Control Hosp Epidemiol. vol. 28. 2007. pp. 1054-1059.

DiazGranados, CA, Zimmer, SM, Klein, M. “Comparison of mortality associated with vancomycin-resistant and vancomycin-susceptible enterococcal bloodstream infections: a meta-analysis”. Clin Infect Dis. vol. 41. 2005. pp. 327-333.

Montecalvo, MA, Horowitz, H, Gedris, C, Carbonaro, C, Tenover, FC, Issah, A, Cook, P, Wormser, GP. “Outbreak of vancomycin-, ampicillin-, and aminoglycoside-resistant Enterococcus faecium bacteremia in an adult oncology unit”. Antimicrob Agents Chemother. vol. 38. 1994 Jun. pp. 1363-7.

Edmond, MB, Ober, JF, Weinbaum, DL, Pfaller, MA, Hwang, T, Sanford, MD, Wenzel, RP. “Vancomycin-resistant Enterococcus faecium bacteremia: risk factors for infection”. Clin Infect Dis. vol. 20. 1995 May. pp. 1126-33.

Hill, EE, Herijgers, P, Claus, P. “Infective endocarditis: changing epidemiology and predictors of 6-month mortality: a prospective cohort study”. Eur Heart J. vol. 28. 2007. pp. 196-203.

Rice, LB, Calderwood, SB, Eliopoulos, GM. “Enterococcal endocarditis: a comparison of prosthetic and native valve disease”. Rev Infect Dis. vol. 13. 1991. pp. 1-17.

Anderson, DJ, Olaison, L, McDonald, JR. “Enterococcal prosthetic valve infective endocarditis: report of 45 episodes from the International Collaboration on Endocarditis-merged database”. Eur J Clin Microbiol Infect Dis. vol. 24. 2005. pp. 665-670.

Fernandez Guerrero, ML, Goyenechea, A, Verdejo, C. “Enterococcal endocarditis on native and prosthetic valves: a review of clinical and prognostic factors with emphasis on hospital-acquired infections as a major determinant of outcome”. Medicine (Baltimore). vol. 86. 2007. pp. 363-377.

Jones, RN, Kugler, KC, Pfaller, MA, Winokur, PL. “Characteristics of pathogens causing urinary tract infections in hospitals in North America: results from the SENTRY Antimicrobial Surveillance Program, 1997”. Diagn Microbiol Infect Dis. vol. 35. 1999. pp. 55-63.

Platt, R, Polk, BF, Murdock, B, Rosner, B. “Mortality associated with nosocomial urinary tract infections”. N Engl J Med. vol. 307. 1982. pp. 637-42.

Krieger, JN, Kaiser, DL, Wenzel, RP. “Urinary tract etiology of bloodstream infections in hospitalized patients”. J Infect Dis. vol. 148. 1983. pp. 57-62.

Heintz, BH, Halilovic, J, Christensen, CL. “Vancomycin-resistant enterococcal urinary tract infections”. Pharmacotherapy. vol. 30. 2010 Nov. pp. 1136-49.

Hidron, AI, Edwards, JR, Patel, J. “NHSN annual update: antimicrobial-resistant pathogens associated with healthcare-associated infections: annual summary of data reported to the National Healthcare Safety Network at the Centers for Disease Control and Prevention, 2006-2007”. Infect Control Hosp Epidemiol. vol. 29. 2008. pp. 996-1011.

Burnett, RJ, Haverstock, DC, Dellinger, EP. “Definition of the role of Enterococcus in intraabdominal infection: analysis of a prospective randomized trial”. Surgery. vol. 118. 1995. pp. 716-721.

Gorbach, SL. “Intraabdominal infections”. Clin Infect Dis. vol. 17. 1993. pp. 961-965.

Harbarth, S, Uckay, I. “Are there patients with peritonitis who require empiric therapy for enterococcus?”. Eur J Clin Microbiol Infect Dis. vol. 23. 2004. pp. 73-77.

Solomkin, JS, Mazuski, JE, Bradley, JS, Rodvold, KA, Goldstein, EJ, Baron, EJ. “Diagnosis and management of complicated intra-abdominal infection in adults and children: guidelines by the Surgical Infection Society and the Infectious Diseases Society of America”. Clin Infect Dis. vol. 50. 2010 Jan 15. pp. 133-64.

Sitges-Serra, A, López, MJ, Girvent, M, Almirall, S, Sancho, JJ. “Postoperative enterococcal infection after treatment of complicated intra-abdominal sepsis”. Br J Surg. vol. 89. 2002 Mar. pp. 361-7.

Kang, CI, Chung, DR, Ko, KS, Peck, KR, Song, JH. “Korean Network for the Study of Infectious Diseases. Clinical predictors for enterococcal bacteraemia in patients with bacteraemic intra-abdominal infections”. Scand J Infect Dis. vol. 42. 2010 Dec. pp. 817-20.

Cercenado, E, Torroba, L, Cantón, R, Martínez-Martínez, L, Chaves, F, García-Rodríguez, JA, Lopez-Garcia, C, Aguilar, L, García-Rey, C, García-Escribano, N, Bouza, E. “Multicenter study evaluating the role of enterococci in secondary bacterial peritonitis”. J Clin Microbiol. vol. 48. 2010. pp. 456-9.

Dhawan, B, Gadepalli, R, Kapil, A. “In vitro activity of daptomycin against Staphylococcus aureus and vancomycin-resistant Enterococcus faecium isolates associated with skin and soft tissue infections: first results from India”. Diagn Microbiol Infect Dis. vol. 65. 2009 Oct. pp. 196-8.

Till, M, Wixson, RL, Pertel, PE. “Linezolid treatment for osteomyelitis due to vancomycin-resistant Enterococcus faecium”. Clin Infect Dis. vol. 34. 2002. pp. 1412-1414.

Stevenson, KB, Murray, EW, Sarubbi, FA. “Enterococcal meningitis: report of four cases and review”. Clin Infect Dis. vol. 18. 1994. pp. 233-9.

Bayer, AS, Seidel, JS, Yoshikawa, TT. “Group D enterococcal meningitis. Clinical and therapeutic considerations with report of three cases and review of the literature”. Arch Intern Med. vol. 136. 1976. pp. 883

Kurup, A, Tee, WS, Loo, LH, Lin, R. “Infection of central nervous system by motile Enterococcus: first case report”. J Clin Microbiol. vol. 39. 2001. pp. 820-2.

Berk, SL, Verghese, A, Holtsclaw, SA, Smith, JK. “Enterococcal pneumonia: occurrence in patients receiving broad spectrum antibiotics and enteral feeding”. Am J Med. vol. 74. 1983. pp. 153-4.

Graham, PL. “Staphylococcal and enterococcal infections in the neonatal intensive care unit”. Semin Perinatol. vol. 26. 2002. pp. 322-331.

Coudron, PE, Mayhall, CG, Facklam, RR. “Streptococcus faecium outbreak in a neonatal intensive care unit”. J Clin Microbiol. vol. 20. 1984. pp. 1044-1048.

Luginbuhl, LM, Rotbart, HA, Facklam, RR. “Neonatal enterococcal sepsis: case-control study and description of an outbreak”. Pediatr Infect Dis J. vol. 6. 1987. pp. 1022-1026.

Dobson, SRM, Baker, CJ. “Enterococcal sepsis in neonates: features by age at onset and occurrence of focal infection”. Pediatrics. vol. 85. 1990. pp. 165-71.

Antibiotic resistance in enterococci

Grayson, ML, Eliopoulos, GM, Wennersten, CB. “Increasing resistance to beta-lactam antibiotics among clinical isolates of Enterococcus faecium: a 22-year review at one institution”. Antimicrob Agents Chemother. vol. 35. 1991. pp. 2180-4.

Oteo, J, Cuevas, O, Navarro, C, Aracil, B, Campos, J. “Trends in antimicrobial resistance in 3469 enterococci isolated from blood (EARSS experience 2001–06, Spain): increasing ampicillin-resistance in Enterococcus faecium”. J Antimicrob Chemother. vol. 59. 2007. pp. 1044-1045.

Fortún, J, Coque, TM, Martín-Dávila, P, Moreno, L, Cantón, R, Loza, E, Baquero, F, Moreno, S. “Risk factors associated with ampicillin resistance in patients with bacteraemia caused by Enterococcus faecium”. J Antimicrob Chemother. vol. 50. 2002. pp. 1003-9.

Mederski-Samoraj, BD, Murray, BE. “High-level resistance to gentamicin in clinical isolates of enterococci”. J Infect Dis. vol. 147. 1983. pp. 751-757.

Chow, JW. “Aminoglycoside resistance in enterococci”. Clin Infect Dis. vol. 31. 2000. pp. 586-589.

Murray, BE. “Vancomycin-resistant enterococcal infections”. N Engl J Med. vol. 342. 2000. pp. 710-21.

Araoka, H, Kimura, M, Yoneyama, A. “A surveillance of high-level gentamicin-resistant enterococcal bacteremia”. J Infect Chemother. 2010 Nov 2.

Chang, CM, Wang, LR, Lee, HC, Lee, NY, Wu, CJ, Ko, WC. “Characterisation of vancomycin-resistant enterococci from hospitalised patients at a tertiary centre over a seven-year period”. J Hosp Infect. vol. 74. 2010 Apr. pp. 377-84.

Protonotariou, E, Dimitroulia, E, Pournaras, S, Pitiriga, V, Sofianou, D, Tsakris, A. “Trends in antimicrobial resistance of clinical isolates of Enterococcus faecalis and Enterococcus faecium in Greece between 2002 and 2007”. J Hosp Infect. vol. 75. 2010 Jul. pp. 225-7.

Brilliantova, AN, Kliasova, GA, Mironova, AV, Tishkov, VI, Novichkova, GA, Bobrynina, VO, Sidorenko, SV. “Spread of vancomycin-resistant Enterococcus faecium in two haematological centres in Russia”. Int J Antimicrob Agents. vol. 35. 2010 Feb. pp. 177-81.

Maillard, O, Corvec, S, Dantal, J, Reynaud, A, Lucet, JC, Bémer, P, Lepelletier, D. “Emergence of high ampicillin-resistant Enterococcus faecium isolates in a kidney transplant ward: role of antibiotic pressure and cross transmission”. Microb Drug Resist. vol. 16. 2010 Jun. pp. 123-8.

Hegstad, K, Mikalsen, T, Coque, TM, Werner, G, Sundsfjord, A. “Mobile genetic elements and their contribution to the emergence of antimicrobial resistant Enterococcus faecalis and Enterococcus faecium”. Clin Microbiol Infect. vol. 16. 2010. pp. 541-554.

Performance standard for antimicrobial susceptibility testing. 2005.

Fontana, R, Ligozzi, M, Pittaluga, F, Satta, G. “Intrinsic penicillin resistance in enterococci”. Microb Drug Resist. vol. 2. 1996. pp. 209

Arias, CA, Murray, BE. “Emergence and management of drug-resistant enterococcal infections”. Expert Rev Anti Infect Ther. vol. 6. 2008 Oct. pp. 637-55.

Murray, BE. “Beta-lactamase-producing enterococci”. Antimicrob Agents Chemother. vol. 36. 1992. pp. 2355-9.

Performance standards for antimicrobial testing: Twentieth informational supplement. 2010.

Rice, LB, Bellais, S, Carias, LL. “Impact of specific pbp5 mutations on expression of beta-lactam resistance in Enterococcus faecium”. Antimicrob Agents Chemother. vol. 48. 2004. pp. 3028

Mainardi, JL, Morel, V, Fourgeaud, M. “Balance between two transpeptidation mechanisms determines the expression of beta-lactam resistance in Enterococcus faecium”. J Biol Chem. vol. 277. 2002. pp. 35801

Moellering, RC, Weinberg, AN. “Studies on antibiotic synergism against enterococci. II. Effect of various antibiotics on the uptake of 14 C-labeled streptomycin by enterococci”. J Clin Invest. vol. 50. 1971. pp. 2580-2584.

Costa, Y, Galimand, M, Leclercq, R, Duval, J, Courvalin, P. “Characterization of the chromosomal aac(6')-Ii gene specific for Enterococcus faecium”. Antimicrob Agents Chemother. vol. 37. 1993 Sep. pp. 1896-903.

Chow, JW, Zervos, MJ, Lerner, SA. “A novel gentamicin resistance gene in Enterococcus”. Antimicrob Agents Chemother. vol. 41. 1997. pp. 511-4.

Rodríguez-Baño, J, Ramírez, E, Muniain, MA, Santos, J, Joyanes, P, González, F, García-Sánchez, M, Martínez-Martínez, L. “Colonization by high-level aminoglycoside-resistant enterococci in intensive care unit patients: epidemiology and clinical relevance”. J Hosp Infect. vol. 60. 2005. pp. 353-9.

Gavaldà, J, Len, O, Miró, JM. “Brief communication: treatment of Enterococcus faecalis endocarditis with ampicillin plus ceftriaxone”. Ann Intern Med. vol. 146. 2007. pp. 574-9.

Tascini, C, Doria, R, Leonildi, A. “Efficacy of the combination ampicillin plus ceftriaxone in the treatment of a case of enterococcal endocarditis due to Enterococcus faecalis highly resistant to gentamicin: efficacy of the "ex vivo" synergism method”. J Chemother. vol. 16. 2004. pp. 400-3.

Leclercq, R, Courvalin, P. “Resistance to glycopeptides in enterococci”. Clin Infect Dis. vol. 24. 1997. pp. 545-54.

Navarro, F, Courvalin, P. “Analysis of genes encoding D-alanine-D-alanine ligase-related enzymes in Enterococcus casseliflavus and Enterococcus flavescens”. Antimicrob Agents Chemother. vol. 38. 1994. pp. 1788-93.

Arthur, M, Courvalin, P. “Genetics and mechanisms of glycopeptide resistance in enterococci”. Antimicrob Agents Chemother. vol. 37. 1993. pp. 1563-71.

San Millan, A, Depardieu, F, Godreuil, S, Courvalin, P. “VanB-type Enterococcus faecium resistant to, dependent on, and constitutively resistant to vancomycin”. Antimicrob Agents Chemother. vol. 53. 2009. pp. 1974-82.

Leclercq, R, Dutka-Malen, S, Duval, J, Courvalin, P. “Vancomycin resistance gene vanC is specific to Enterococcus gallinarum”. Antimicrob Agents Chemother. vol. 36. 1992. pp. 2005-8.

Dutka-Malen, S, Evers, S, Courvalin, P. “Detection of glycopeptide resistance genotypes and identification to the species level of clinically relevant enterococci by PCR”. J Clin Microbiol. vol. 33. 1995. pp. 1434

Fines, M, Perichon, B, Reynolds, P. “VanE, a new type of acquired glycopeptide resistance in Enterococcus faecalis BM4405”. Antimicrob Agents Chemother. vol. 43. 1999. pp. 2161-4.

Boyd, DA, Willey, BM, Fawcett, D. “Molecular characterization of Enterococcus faecalis N06-0364 with low-level vancomycin resistance harboring a novel D-Ala-D-Ser gene cluster, vanL”. Antimicrob Agents Chemother. vol. 52. 2008. pp. 2667-72.

Guardabassi, L, Agersø, Y. “Genes homologous to glycopeptide resistance vanA are widespread in soil microbial communities”. FEMS Microbiol Lett. vol. 259. 2006. pp. 221-5.

Foucault, ML, Depardieu, F, Courvalin, P, Grillot-Courvalin, C. “Inducible expression eliminates the fitness cost of vancomycin resistance in enterococci”. Proc Natl Acad Sci U S A. vol. 107. 2010 Sep 28. pp. 16964-9.

Performance Standards for Antimicrobial Susceptibility Testing: Sixteenth Informational Supplement. M100-S16 Methods for dilution antimicrobial susceptibility tests for bacteria that grow aerobically: Approved Standard. vol. 26. 2006.

San Millan, A, Depardieu, F, Godreuil, S, Courvalin, P. “VanB-type Enterococcus faecium clinical isolate successively inducibly resistant to, dependent on, and constitutively resistant to vancomycin”. Antimicrob Agents Chemother. vol. 53. 2009. pp. 1974-82.

Reynolds, PE. “Structure, biochemistry and mechanism of action of glycopeptide antibiotics”. Eur J Clin Microbiol Infect Dis. vol. 8. 1989. pp. 943-50.

Rippere, K, Patel, R, Uhl, JR, Piper, KE, Steckelberg, JM, Kline, BC, Cockerill, FR, Yousten, AA. “DNA sequence resembling vanA and vanB in the vancomycin-resistant biopesticide Bacillus popilliae”. J Infect Dis. vol. 178. 1998 Aug. pp. 584-8.

Stinear, TP, Olden, DC, Johnson, PD, Davies, JK, Grayson, ML. “Enterococcal vanB resistance locus in anaerobic bacteria in human faeces”. Lancet. vol. 357. 2001 Mar 17. pp. 855-6.

Poyart, C, Pierre, C, Quesne, G, Pron, B, Berche, P, Trieu-Cuot, P. “Emergence of vancomycin resistance in the genus Streptococcus: characterization of a vanB transferable determinant in Streptococcus bovis”. Antimicrob Agents Chemother. vol. 41. 1997 Jan. pp. 24-9.

Biavasco, F, Giovanetti, E, Miele, A, Vignaroli, C, Facinelli, B, Varaldo, PE. “In vitro conjugative transfer of VanA vancomycin resistance between Enterococci and Listeriae of different species”. Eur J Clin Microbiol Infect Dis. vol. 15. 1996 Jan. pp. 50-9.

Patel, R, Piper, K, Cockerill, FR. “The biopesticide Paenibacillus popilliae has a vancomycin resistance gene cluster homologous to the enterococcal vanA vancomycin resistance gene cluster”. Antimicrob Agents Chemother. vol. 44. 2000. pp. 705

Guardabassi, L, Christensen, H, Hasman, H, Dalsgaard, A. “Members of the genera Paenibacillus and Rhodococcus harbor genes homologous to enterococcal glycopeptide resistance genes vanA and vanB”. Antimicrob Agents Chemother. vol. 48. 2004. pp. 4915

Chang, S, Sievert, DM, Hageman, JC. “Infection with vancomycin-resistant Staphylococcus aureus containing the vanA resistance gene”. N Engl J Med. vol. 348. 2003. pp. 1342-7.

Werner, G, Coque, TM, Hammerum, AM, Hope, R, Hryniewicz, W, Johnson, A. “Emergence and spread of vancomycin resistance among enterococci in Europe”. Euro Surveill. vol. 13. 2008 Nov 20. pp. 19046

Bourdon, N, Fines-Guyon, M, Thiolet, JM, Maugat, S, Coignard, B, Leclercq, R, Cattoir, V. “Changing trends in vancomycin-resistant enterococci in French hospitals, 2001-08”. J Antimicrob Chemother. vol. 66. 2011 Apr. pp. 713-21.

Grayson, ML, Thauvin-Eliopoulos, C, Eliopoulos, GM. “Failure of trimethoprim-sulfamethoxazole therapy in experimental enterococcal endocarditis”. Antimicrob Agents Chemother. vol. 34. 1990. pp. 1792-4.

Singh, KV, Weinstock, GM, Murray, BE. “An Enterococcus faecalis ABC homologue (Lsa) is required for the resistance of this species to clindamycin and quinupristin-dalfopristin”. Antimicrob Agents Chemother. vol. 46. 2002. pp. 1845-50.

Kehrenberg, C, Schwarz, S, Jacobsen, L. “A new mechanism for chloramphenicol, florfenicol and clindamycin resistance: methylation of 23S ribosomal RNA at A2503”. Mol Microbiol. vol. 57. 2005. pp. 1064-73.

Werner, G, Fleige, C, Ewert, B, Laverde-Gomez, JA, Klare, I, Witte, W. “High-level ciprofloxacin resistance among hospital-adapted Enterococcus faecium (CC17)”. Int J Antimicrob Agents. vol. 35. 2010 Feb. pp. 119-25.

Meka, VG, Gold, HS. “Antimicrobial resistance to linezolid”. Clin Infect Dis. vol. 39. 2004. pp. 1010-5.

Dobbs, TE, Patel, M, Waites, KB. “Nosocomial spread of Enterococcus faecium resistant to vancomycin and linezolid in a tertiary care medical center”. J Clin Microbiol. vol. 44. 2006. pp. 3368-70.

Raad, II, Hanna, HA, Hachem, RY. “Clinical-use-associated decrease in susceptibility of vancomycin-resistant Enterococcus faecium to linezolid: a comparison with quinupristin-dalfopristin”. Antimicrob Agents Chemother. vol. 48. 2004. pp. 3583-5.

Pogue, JM, Paterson, DL, Pasculle, AW, Potoski, BA. “Determination of risk factors associated with isolation of linezolid-resistant strains of vancomycin-resistant Enterococcus”. Infect Control Hosp Epidemiol. vol. 28. 2007. pp. 1382-8.

Bourgeois-Nicolaos, N, Massias, L, Couson, B. “Dose dependence of emergence of resistance to linezolid in Enterococcus faecalis in vivo”. J Infect Dis. vol. 195. 2007. pp. 1480-8.

Arias, CA, Vallejo, M, Reyes, J. “Clinical and microbiological aspects of linezolid resistance mediated by the cfr gene encoding a 23S rRNA methyltransferase”. J Clin Microbiol. vol. 46. 2008. pp. 892-6.

Prystowsky, J, Siddiqui, F, Chosay, J. “Resistance to linezolid: characterization of mutations in rRNA and comparison of their occurrences in vancomycin-resistant enterococci”. Antimicrob Agents Chemother. vol. 45. 2001. pp. 2154-6.

Herrero, IA, Issa, NC, Patel, R. “Nosocomial spread of linezolid-resistant, vancomycin-resistant Enterococcus faecium”. N Engl J Med. vol. 346. 2002. pp. 867-9.

Gonzales, RD, Schreckenberger, PC, Graham, MB. “Infections due to vancomycin-resistant Enterococcus faecium resistant to linezolid”. Lancet. vol. 357. 2001. pp. 1179

Spiliopoulou, I, Damani, A, Chini, V, Zerva, L, Kolonitsiou, F, Anastassiou, ED, Petinaki, E. “Linezolid-Resistant Enterococci in Greece: Epidemiological Characteristics”. Chemotherapy. vol. 57. 2011 Apr 6. pp. 181-185.

Schnitzler, P, Schulz, K, Lampson, C, Geiss, M, Geiss, HK. “Molecular analysis of linezolid resistance in clinical Enterococcus faecium isolates by polymerase chain reaction and pyrosequencing”. Eur J Clin Microbiol Infect Dis. vol. 30. 2011 Jan. pp. 121-5.

Arbeit, RD, Maki, D, Tally, FP. “The safety and efficacy of daptomycin for the treatment of complicated skin and skin-structure infections”. Clin Infect Dis. vol. 38. 2004. pp. 1673-81.

Poutsiaka, DD, Skiffington, S, Miller, KB. “Daptomycin in the treatment of vancomycin-resistant Enterococcus faecium bacteremia in neutropenic patients”. J Infect. vol. 54. 2007. pp. 567-71.

Arias, CA, Torres, HA, Singh, KV. “Failure of daptomycin monotherapy for endocarditis caused by an Enterococcus faecium strain with vancomycin-resistant and vancomycin-susceptible subpopulations and evidence of in vivo loss of the vanA gene cluster”. Clin Infect Dis. vol. 45. 2007. pp. 1343-6.

Lewis, JS, Owens, A, Cadena, J, Sabol, K, Patterson, JE, Jorgensen, JH. “Emergence of daptomycin resistance in Enterococcus faecium during daptomycin therapy”. Antimicrob Agents Chemother. vol. 49. 2005. pp. 1664-65.

Cantón, R, Ruiz-Garbajosa, P, Chaves, RL, Johnson, AP. “A potential role for daptomycin in enterococcal infections: what is the evidence?”. J Antimicrob Chemother. vol. 65. 2010 Jun. pp. 1126-36.

Kainer, MA, Devasia, RA, Jones, TF, Simmons, BP, Meltouk, K, Chow, S. “Response to emerging infection leading to outbreak of linezolid-resistant enterococci”. Emerg Infect Dis. vol. 13. 2007. pp. 1024-1030.

Sader, HS, Moet, GJ, Farrell, DJ, Jones, RN. “Antimicrobial susceptibility of daptomycin and comparator agents tested against methicillin-resistant Staphylococcus aureus and vancomycin-resistant enterococci: trend analysis of a 6-year period in US medical centers (2005-2010)”. Diagn Microbiol Infect Dis. 2011 May 3.

Kelesidis, T, Humphries, R, Uslan, DZ, Pegues, DA. “Daptomycin nonsusceptible enterococci: an emerging challenge for clinicians”. Clin Infect Dis. vol. 52. 2011 Jan 15. pp. 228-34.

Moellering, RC, Linden, PK, Reinhardt, J. “The efficacy and safety of quinupristin/dalfopristin for the treatment of infections caused by vancomycin-resistant Enterococcus faecium. Synercid Emergency-Use Study Group”. J Antimicrob Chemother. vol. 44. 1999. pp. 251-61.

McDonald, LC, Rossiter, S, Mackinson, C. “Quinupristin-dalfopristin-resistant Enterococcus faecium on chicken and in human stool specimens”. N Engl J Med. vol. 345. 2001. pp. 1155-60.

Hershberger, E, Donabedian, S, Konstantinou, K, Zervos, MJ. “Quinupristin-dalfopristin resistance in gram-positive bacteria: mechanism of resistance and epidemiology”. Clin Infect Dis. vol. 38. 2004. pp. 92-8.

Kehoe, LE, Snidwongse, J, Courvalin, P. “Structural basis of Synercid (quinupristin-dalfopristin) resistance in Gram-positive bacterial pathogens”. J Biol Chem. vol. 278. 2003. pp. 29963-70.

Werner, G, Gfrörer, S, Fleige, C. “Tigecycline-resistant Enterococcus faecalis strain isolated from a German intensive care unit patient”. J Antimicrob Chemother. vol. 61. 2008. pp. 1182-3.

Zhanel, GG, Calic, D, Schweizer, F, Zelenitsky, S, Adam, H, Lagacé-Wiens, PR, Rubinstein, E, Gin, AS, Hoban, DJ, Karlowsky, JA. “New lipoglycopeptides: a comparative review of dalbavancin, oritavancin and telavancin”. Drugs. vol. 70. 2010. pp. 859-86.

Epidemiology of VRE

McBryde, ES, McElwain, DL. “A mathematical model investigating the impact of an environmental reservoir on the prevalence and control of vancomycin-resistant enterococci”. J Infect Dis. vol. 193. 2006 May 15. pp. 1473-4.

Pearman, JW. “2004 Lowbury Lecture: the Western Australian experience with vancomycin-resistant enterococci – from disaster to ongoing control”. J Hosp Infect. vol. 63. 2006 May. pp. 14-26.

Mascini, EM, Troelstra, A, Beitsma, M, Blok, HE, Jalink, KP, Hopmans, TE, Fluit, AC, Hene, RJ, Willems, RJ, Verhoef, J, Bonten, MJ. “Genotyping and preemptive isolation to control an outbreak of vancomycin-resistant Enterococcus faecium”. Clin Infect Dis. vol. 42. 2006 Mar 15. pp. 739-46.

Gearhart, M, Martin, J, Rudich, S, Thomas, M, Wetzel, D, Solomkin, J, Hanaway, MJ, Aranda-Michel, J, Weber, F, Trumball, L, Bass, M, Zavala, E, Steve Woodle, E, Buell, JF. “Consequences of vancomycin-resistant Enterococcus in liver transplant recipients: a matched control study”. Clin Transplant. vol. 19. 2005. pp. 711-6.

Armeanu, E, Bonten, MJ. “Control of vancomycin-resistant enterococci: one size fits all?”. Clin Infect Dis. vol. 41. 2005 Jul 15. pp. 210-6.

Ergaz, Z, Arad, I, Bar-Oz, B, Peleg, O, Benenson, S, Minster, N, Moses, A, Block, C. “Elimination of vancomycin-resistant enterococci from a neonatal intensive care unit following an outbreak”. J Hosp Infect. vol. 74. 2010 Apr. pp. 370-6.

Milstone, AM, Maragakis, LL, Carroll, KC, Perl, TM. “Targeted surveillance to identify children colonized with vancomycin-resistant Enterococcus in the pediatric intensive care unit”. Infect Control Hosp Epidemiol. vol. 31. 2010 Jan. pp. 95-8.

Kamboj, M, Chung, D, Seo, SK, Pamer, EG, Sepkowitz, KA, Jakubowski, AA, Papanicolaou, G. “The changing epidemiology of vancomycin-resistant Enterococcus (VRE) bacteremia in allogeneic hematopoietic stem cell transplant (HSCT) recipients”. Biol Blood Marrow Transplant. vol. 16. 2010 Nov. pp. 1576-81.

Tschudin Sutter, S, Frei, R, Dangel, M, Gratwohl, A, Bonten, M, Widmer, AF. “Not all patients with vancomycin-resistant enterococci need to be isolated”. Clin Infect Dis. vol. 51. 2010 Sep 15. pp. 678-83.

Reyes, K, Malik, R, Moore, C, Donabedian, S, Perri, M, Johnson, L, Zervos, M. “Evaluation of risk factors for coinfection or cocolonization with vancomycin-resistant enterococcus and methicillin-resistant Staphylococcus aureus”. J Clin Microbiol. vol. 48. 2010 Feb. pp. 628-30.

Mikulska, M, Del Bono, V, Prinapori, R, Boni, L, Raiola, AM, Gualandi, F, Van Lint, MT, Dominietto, A, Lamparelli, T, Cappellano, P, Bacigalupo, A, Viscoli, C. “Risk factors for enterococcal bacteremia in allogeneic hematopoietic stem cell transplant recipients”. Transpl Infect Dis. vol. 12. 2010 Dec. pp. 505-12.

Fallico, L, Boldrin, C, Grossato, A, Franchin, E, De Canale, E, Tommasini, T, Parisi, SG, Manganelli, R, Palù, G. “Molecular epidemiology of Enterococcus faecium isolates from an Italian hospital”. Infection. vol. 39. 2011 Apr. pp. 127-33.

Ramsey, AM, Zilberberg, MD. “Secular trends of hospitalization with vancomycin-resistant enterococcus infection in the United States, 2000-2006”. Infect Control Hosp Epidemiol. vol. 30. 2009. pp. 184-6.

Nguyen, GC, Leung, W, Weizman, AV. “Increased risk of vancomycin-resistant enterococcus (VRE) infection among patients hospitalized for inflammatory bowel disease in the United States”. Inflamm Bowel Dis. 2010 Nov 8.

Lee, WG, Park, IJ, Jin, HY, Park, MH. “Relapse and reacquisition of rectal colonization by vancomycin-resistant Enterococcus faecium after decolonization”. Epidemiol Infect. vol. 138. 2010 Oct. pp. 1449-53.

Bonten, MJ, Slaughter, S, Ambergen, AW. “The role of "colonization pressure" in the spread of vancomycin-resistant enterococci: an important infection control variable”. Arch Intern Med. vol. 158. 1998. pp. 1127-32.

Pereira, GH, Müller, PR, Zanella, RC, de Jesus Castro Lima, M, Torchio, DS, Levin, AS. “Outbreak of vancomycin-resistant enterococci in a tertiary hospital: the lack of effect of measures directed mainly by surveillance cultures and differences in response between Enterococcus faecium and Enterococcus faecalis”. Am J Infect Control. vol. 38. 2010 Jun. pp. 406-9.

Haas, EJ, Zaoutis, TE, Prasad, P, Li, M, Coffin, SE. “Risk Factors and Outcomes for Vancomycin-Resistant Enterococcus Bloodstream Infection in Children”. Infect Control Hosp Epidemiol. 2010 Aug 31.

Wang, LJ, Hsueh, PR. “Therapeutic options for infections due to vancomycin – resistant enterococci”. Expert Opin Pharmacother. vol. 10. 2009. pp. 785-96.

Coque, TM, Tomayko, JF, Ricke, SC, Okhyusen, PC, Murray, BE. “Vancomycin-resistant enterococci from nosocomial, community, and animal sources in the United States”. Antimicrob Agents Chemother. vol. 40. 1996 Nov. pp. 2605-9.

Donabedian, SM, Perri, MB, Abdujamilova, N, Gordoncillo, MJ, Naqvi, A, Reyes, KC, Zervos, MJ, Bartlett, P. “Characterization of vancomycin-resistant Enterococcus faecium isolated from swine in three Michigan counties”. J Clin Microbiol. vol. 48. 2010 Nov. pp. 4156-60.

Uttley, AH, George, RC, Naidoo, J. “High-level vancomycin-resistant enterococci causing hospital infections”. Epidemiol Infect. vol. 103. 1989. pp. 173-81.

Leclercq, R, Derlot, E, Duval, J, Courvalin, P. “Plasmid-mediated resistance to vancomycin and teicoplanin in Enterococcus faecium”. N Engl J Med. vol. 319. 1988. pp. 157-61.

Murray, BE. “What can we do about vancomycin-resistant enterococci?”. Clin Infect Dis. vol. 20. 1995 May. pp. 1134-6.

Thal, LA, Chow, JW, Mahayni, R, Bonilla, H, Perri, MB, Donabedian, SA, Silverman, J, Taber, S, Zervos, MJ. “Characterization of antimicrobial resistance in enterococci of animal origin”. Antimicrob Agents Chemother. vol. 39. 1995 Sep. pp. 2112-5.

Bates, J, Jordens, JZ, Griffiths, DT. “Farm animals as a putative reservoir for vancomycin-resistant enterococcal infection in man”. J Antimicrob Chemother. vol. 34. 1994 Oct. pp. 507-14.

Klare, I, Heier, H, Claus, H, Böhme, G, Marin, S, Seltmann, G, Hakenbeck, R, Antanassova, V, Witte, W. “Enterococcus faecium strains with vanA-mediated high-level glycopeptide resistance isolated from animal foodstuffs and fecal samples of humans in the community”. Microb Drug Resist. vol. 1. 1995 Fall. pp. 265-72.

Wegener, HC, Aarestrup, FM, Jensen, LB, Hammerum, AM, Bager, F. “Use of antimicrobial growth promoters in food animals and Enterococcus faecium resistance to therapeutic antimicrobial drugs in Europe”. Emerg Infect Dis. vol. 5. 1999 May-Jun. pp. 329-35.

Klare, I, Badstübner, D, Konstabel, C, Böhme, G, Claus, H, Witte, W. “Decreased incidence of VanA-type vancomycin-resistant enterococci isolated from poultry meat and from fecal samples of humans in the community after discontinuation of avoparcin usage in animal husbandry”. Microb Drug Resist. vol. 5. 1999 Spring. pp. 45-52.

Pantosti, A, Del Grosso, M, Tagliabue, S, Macrì, A, Caprioli, A. “Decrease of vancomycin-resistant enterococci in poultry meat after avoparcin ban”. Lancet. vol. 354. 1999 Aug 28. pp. 741-2.

Simonsen, GS, Haaheim, H, Dahl, KH, Kruse, H, Løvseth, A, Olsvik, O, Sundsfjord, A. “Transmission of VanA-type vancomycin-resistant enterococci and vanA resistance elements between chicken and humans at avoparcin-exposed farms”. Microb Drug Resist. vol. 4. 1998 Winter. pp. 313-8.

Ajao, AO, Harris, AD, Roghmann, MC, Johnson, JK, Zhan, M, McGregor, JC, Furuno, JP. “Systematic review of measurement and adjustment for colonization pressure in studies of methicillin-resistant Staphylococcus aureus, vancomycin-resistant enterococci, and clostridium difficile acquisition”. Infect Control Hosp Epidemiol. vol. 32. 2011 May. pp. 481-9.

Lin, MY, Hayden, MK. “Methicillin-resistant Staphylococcus aureus and vancomycin-resistant enterococcus: recognition and prevention in intensive care units”. Crit Care Med. vol. 38. 2010 Aug. pp. S335-44.

Donabedian, SM, Perri, MB, Abdujamilova, N, Gordoncillo, MJ, Naqvi, A, Reyes, KC, Zervos, MJ, Bartlett, P. “Characterization of vancomycin-resistant Enterococcus faecium isolated from swine in three Michigan counties”. J Clin Microbiol. vol. 48. 2010 Nov. pp. 4156-60.

Zanella, RC, Valdetaro, F, Lovgren, M, Tyrrel, GJ, Bokermann, S, Almeida, SC, Vieira, VS, Brandileone, MC. “First confirmed case of a vancomycin-resistant Enterococcus faecium with vanA phenotype from Brazil: isolation from a meningitis case in São Paulo”. Microb Drug Resist. vol. 5. 1999 Summer. pp. 159-62.

Aarestrup, FM, Agerso, Y, Gerner-Smidt, P, Madsen, M, Jensen, LB. “Comparison of antimicrobial resistance phenotypes and resistance genes in Enterococcus faecalis and Enterococcus faecium from humans in the community, broilers, and pigs in Denmark”. Diagn Microbiol Infect Dis. vol. 37. 2000 Jun. pp. 127-37.

Low, DE, Keller, N, Barth, A, Jones, RN. “Clinical prevalence, antimicrobial susceptibility, and geographic resistance patterns of enterococci: results from the SENTRY Antimicrobial Surveillance Program, 1997-1999”. Clin Infect Dis. vol. 32. 2001 May 15. pp. S133-45.

von Gottberg, A, van Nierop, W, Dusé, A, Kassel, M, McCarthy, K, Brink, A, Meyers, M, Smego, R, Koornhof, H. “Epidemiology of glycopeptide-resistant enterococci colonizing high-risk patients in hospitals in Johannesburg, Republic of South Africa”. J Clin Microbiol. vol. 38. 2000 Feb. pp. 905-9.

Karlowsky, JA, Zhanel, GG, Hoban, DJ. “Vancomycin-resistant enterococci (VRE) colonization of high-risk patients in tertiary care Canadian hospitals. Canadian VRE Surveillance Group”. Diagn Microbiol Infect Dis. vol. 35. 1999 Sep. pp. 1-7.

Hsueh, PR, Teng, LJ, Pan, HJ, Chen, YC, Wang, LH, Chang, SC, Ho, SW, Luh, KT. “Emergence of vancomycin-resistant enterococci at a university hospital in Taiwan: persistence of multiple species and multiple clones”. Infect Control Hosp Epidemiol. vol. 20. 1999 Dec. pp. 828-33.

Brown, DF, Hope, R, Livermore, DM. “Non-susceptibility trends among enterococci and non-pneumococcal streptococci from bacteraemias in the UK and Ireland, 2001–06”. J Antimicrob Chemother. vol. 62. 2008. pp. ii75-ii85.

Karanfil, LV, Murphy, M, Josephson, A. “A cluster of vancomycin-resistant Enterococcus faecium in an intensive care unit”. Infect Control Hosp Epidemiol. vol. 13. 1992. pp. 195-200.

Rubin, LG, Tucci, V, Cercenado, E. “Vancomycin-resistant Enterococcus faecium in hospitalized children”. Infect Control Hosp Epidemiol. vol. 13. 1992. pp. 700-5.

Handwerger, S, Raucher, B, Altarac, D. “Nosocomial outbreak due to Enterococcus faecium highly resistant to vancomycin, penicillin, and gentamicin”. Clin Infect Dis. vol. 16. 1993. pp. 750-5.

Boyce, JM, Opal, SM, Chow, JW. “Outbreak of multidrug-resistant Enterococcus faecium with transferable vanB class vancomycin resistance”. J Clin Microbiol. vol. 35. 1994. pp. 1148-53.

Ostrowsky, BE, Trick, WE, Sohn, AH. “Control of vancomycin-resistant enterococcus in health care facilities in a region”. N Engl J Med. vol. 344. 2001. pp. 1427-33.

Miranda, AG, Singh, KV, Murray, BE. “DNA fingerprinting of Enterococcus faecium by pulsed-field gel electrophoresis may be a useful epidemiologic tool”. J Clin Microbiol. vol. 29. 1991. pp. 2752-7.

Boyle, JF, Soumakis, SA, Rendo, A. “Epidemiologic analysis and genotypic characterization of a nosocomial outbreak of vancomycin-resistant enterococci”. J Clin Microbiol. vol. 31. 1993. pp. 1280-5.

Morris, JG, Shay, DK, Hebden, JN. “Enterococci resistant to multiple antimicrobial agents, including vancomycin. Establishment of endemicity in a university medical center”. Ann Intern Med. vol. 123. 1995. pp. 250-9.

Johnson, PD, Ballard, SA, Grabsch, EA, Stinear, TP, Seemann, T, Young, HL, Grayson, ML, Howden, BP. “A sustained hospital outbreak of vancomycin-resistant Enterococcus faecium bacteremia due to emergence of vanB E. faecium sequence type 203”. J Infect Dis. vol. 202. 2010 Oct 15. pp. 1278-86.

Altoparlak, U, Koca, O, Ozkurt, Z, Akcay, MN. “Incidence and risk factors of vancomycin-resistant enterococcus colonization in burn unit patients”. Burns. vol. 37. 2011 Feb. pp. 49-53.

Moretti, ML, de Oliveira Cardoso, LG, Levy, CE, Von Nowakosky, A, Bachur, LF, Bratfich, O, Leichsenring, ML, Fagnani, R, Peres Evangelista Dantas, SM, Resende, MR, Trabasso, P. “Controlling a vancomycin-resistant enterococci outbreak in a Brazilian teaching hospital”. Eur J Clin Microbiol Infect Dis. vol. 30. 2011 Mar. pp. 369-74.

Almyroudis, NG, Lesse, AJ, Hahn, T, Samonis, G, Hazamy, PA, Wongkittiroch, K, Wang, ES, McCarthy, PL, Wetzler, M, Segal, BH. “Molecular epidemiology and risk factors for colonization by vancomycin-resistant Enterococcus in patients with hematologic malignancies”. Infect Control Hosp Epidemiol. vol. 32. 2011 May. pp. 490-6.

Furtado, GH, Mendes, RE, Pignatari, AC, Wey, SB, Medeiros, EA. “Risk factors for vancomycin-resistant Enterococcus faecalis bacteremia in hospitalized patients: an analysis of two case-control studies”. Am J Infect Control. vol. 34. 2006 Sep. pp. 447-51.

Farr, BM. “What to think if the results of the National Institutes of Health randomized trial of methicillin-resistant Staphylococcus aureus and vancomycin-resistant enterococcus control measures are negative (and other advice to young epidemiologists): a review and an au revoir”. Infect Control Hosp Epidemiol. vol. 27. 2006 Oct. pp. 1096-106.

Sigurdardottir, B, Berg, JV, Hu, J, Alamu, J, McNutt, LA, Diekema, DJ, Herwaldt, LA. “Descriptive epidemiology and case-control study of patients colonized with vancomycin-resistant enterococcus and methicillin-resistant Staphylococcus aureus”. Infect Control Hosp Epidemiol. vol. 27. 2006 Sep. pp. 913-9.

Donskey, CJ, Chowdhry, TK, Hecker, MT. “Effect of antibiotic therapy on the density of vancomycin-resistant enterococci in the stool of colonized patients”. N Engl J Med. vol. 343. 2000. pp. 1925-32.

D’Agata, EM, Gautam, S, Green, WK, Tang, YW. “High rate of false-negative results of the rectal swab culture method in detection of gastrointestinal colonization with vancomycin-resistant enterococci”. Clin Infect Dis. vol. 34. 2002. pp. 167-72.

Livornese, LL, Dias, S, Samel, C. “Hospital-acquired infection with vancomycin-resistant Enterococcus faecium transmitted by electronic thermometers”. Ann Intern Med. vol. 117. 1992. pp. 112-6.

Noskin, GA, Stosor, V, Cooper, I, Peterson, LR. “Recovery of vancomycin-resistant enterococci on fingertips and environmental surfaces”. Infect Control Hosp Epidemiol. vol. 16. 1995. pp. 577-81.

Gordts, B, Van Landuyt, H, Ieven, M, Vandamme, P, Goossens, H. “Vancomycin-resistant enterococci colonizing the intestinal tracts of hospitalized patients”. J Clin Microbiol. vol. 33. 1995 Nov. pp. 2842-6.

Montecalvo, MA, de Lencastre, H, Carraher, M, Gedris, C, Chung, M, VanHorn, K, Wormser, GP. “Natural history of colonization with vancomycin-resistant Enterococcus faecium”. Infect Control Hosp Epidemiol. vol. 16. 1995 Dec. pp. 680-5.

Moreno, F, Grota, P, Crisp, C, Magnon, K, Melcher, GP, Jorgensen, JH, Patterson, JE. “Clinical and molecular epidemiology of vancomycin-resistant Enterococcus faecium during its emergence in a city in southern Texas”. Clin Infect Dis. vol. 21. 1995 Nov. pp. 1234-7.

Shay, DK, Goldmann, DA, Jarvis, WR. “Reducing the spread of antimicrobial-resistant microorganisms. Control of vancomycin-resistant enterococci”. Pediatr Clin North Am. vol. 42. 1995 Jun. pp. 703-16.

Wells, CL, Juni, BA, Cameron, SB, Mason, KR, Dunn, DL, Ferrieri, P, Rhame, FS. “Stool carriage, clinical isolation, and mortality during an outbreak of vancomycin-resistant enterococci in hospitalized medical and/or surgical patients”. Clin Infect Dis. vol. 21. 1995 Jul. pp. 45-50.

Lam, S, Singer, C, Tucci, V, Morthland, VH, Pfaller, MA, Isenberg, HD. “The challenge of vancomycin-resistant enterococci: a clinical and epidemiologic study”. Am J Infect Control. vol. 23. 1995 Jun. pp. 170-80.

Boyce, JM, Opal, SM, Chow, JW, Zervos, MJ, Potter-Bynoe, G, Sherman, CB, Romulo, RL, Fortna, S, Medeiros, AA. “Outbreak of multidrug-resistant Enterococcus faecium with transferable vanB class vancomycin resistance”. J Clin Microbiol. vol. 32. 1994 May. pp. 1148-53.

Weinstein, JW, Roe, M, Towns, M. “Resistant enterococci: a prospective study of prevalence, incidence, and factors associated with colonization in a university hospital”. Infect Control Hosp Epidemiol. vol. 17. 1996. pp. 36-41.

Riedel, S, Von Stein, D, Richardson, K. “Development of a prediction rule for methicillin-resistant Staphylococcus aureus and vancomycin-resistant enterococcus carriage in a Veterans Affairs Medical Center population”. Infect Control Hosp Epidemiol. vol. 29. 2008. pp. 969-71.

Cohen, MJ, Adler, A, Block, C. “Acquisition of vancomycin-resistant enterococci in internal medicine wards”. Am J Infect Control. vol. 37. 2009. pp. 111-6.

Elizaga, ML, Weinstein, RA, Hayden, MK. “Patients in long-term care facilities: a reservoir for vancomycin-resistant enterococci”. Clin Infect Dis. vol. 34. 2002. pp. 441-6.

Fridkin, SK, Edwards, JR, Courval, JM. “The effect of vancomycin and third-generation cephalosporins on prevalence of vancomycin-resistant enterococci in 126 U.S. adult intensive care units”. Ann Intern Med. vol. 135. 2001. pp. 175-83.

Brandl, K, Plitas, G, Mihu, CN, Ubeda, C, Jia, T, Fleisher, M, Schnabl, B, DeMatteo, RP, Pamer, EG. “Vancomycin-resistant enterococci exploit antibiotic-induced innate immune deficits”. Nature. vol. 455. 2008 Oct 9. pp. 804-7.

Ray, AJ, Hoyen, CK, Taub, TF. “Nosocomial transmission of vancomycin-resistant enterococci from surfaces”. JAMA. vol. 287. 2002. pp. 1400-1.

Porwancher, R, Sheth, A, Remphrey, S. “Epidemiological study of hospital-acquired infection with vancomycin-resistant Enterococcus faecium: possible transmission by an electronic ear-probe thermometer”. Infect Control Hosp Epidemiol. vol. 18. 1997. pp. 771-3.

Trillis, F, Eckstein, EC, Budavich, R. “Contamination of hospital curtains with healthcare-associated pathogens”. Infect Control Hosp Epidemiol. vol. 29. 2008. pp. 1074-6.

Martínez, JA, Ruthazer, R, Hansjosten, K. “Role of environmental contamination as a risk factor for acquisition of vancomycin-resistant enterococci in patients treated in a medical intensive care unit”. Arch Intern Med. vol. 163. 2003. pp. 1905-12.

Duckro, AN, Blom, DW, Lyle, EA. “Transfer of vancomycin-resistant enterococci via health care worker hands”. Arch Intern Med. vol. 165. 2005. pp. 302-7.

Hayden, MK, Bonten, MJ, Blom, DW. “Reduction in acquisition of vancomycin-resistant enterococcus after enforcement of routine environmental cleaning measures”. Clin Infect Dis. vol. 42. 2006. pp. 1552-60.

Boyce, JM, Mermel, LA, Zervos, MJ, Rice, LB, Potter-Bynoe, G, Giorgio, C, Medeiros, AA. “Controlling vancomycin-resistant enterococci”. Infect Control Hosp Epidemiol. vol. 16. 1995 Nov. pp. 634-7.

Hota, B, Blom, DW, Lyle, EA. “Interventional evaluation of environmental contamination by vancomycin-resistant enterococci: failure of personnel, product, or procedure?”. J Hosp Infect. vol. 71. 2009. pp. 123-31.

Montecalvo, MA, Jarvis, WR, Uman, J. “Infection-control measures reduce transmission of vancomycin-resistant enterococci in an endemic setting”. Ann Intern Med. vol. 131. 1999. pp. 269-72.

May, AK, Melton, SM, McGwin, G. “Reduction of vancomycin-resistant enterococcal infections by limitation of broad-spectrum cephalosporin use in a trauma and burn intensive care unit”. Shock. vol. 14. 2000. pp. 259-64.

Price, CS, Paule, S, Noskin, GA, Peterson, LR. “Active surveillance reduces the incidence of vancomycin-resistant enterococcal bacteremia”. Clin Infect Dis. vol. 37. 2003. pp. 921-8.

Calfee, DP, Giannetta, ET, Durbin, LJ. “Control of endemic vancomycin-resistant Enterococcus among inpatients at a university hospital”. Clin Infect Dis. vol. 37. 2003. pp. 326-32.

Perencevich, EN, Fisman, DN, Lipsitch, M. “Projected benefits of active surveillance for vancomycin-resistant enterococci in intensive care units”. Clin Infect Dis. vol. 38. 2004. pp. 1108-15.

Huang, SS, Rifas-Shiman, SL, Pottinger, JM. “Improving the assessment of vancomycin-resistant enterococci by routine screening”. J Infect Dis. vol. 195. 2007. pp. 339-46.

Johnston, BL, Bryce, E. “Hospital infection control strategies for vancomycin-resistant Enterococcus, methicillin-resistant Staphylococcus aureus and Clostridium difficile”. CMAJ. vol. 180. 2009 Mar 17. pp. 627-31.

Morris-Downes, M, Smyth, EG, Moore, J, Thomas, T, Fitzpatrick, F, Walsh, J, Caffrey, V, Morris, A, Foley, S, Humphreys, H. “Surveillance and endemic vancomycin-resistant enterococci: some success in control is possible”. J Hosp Infect. vol. 75. 2010 Jul. pp. 228-33.

Aumeran, C, Baud, O, Lesens, O, Delmas, J, Souweine, B, Traoré, O. “Successful control of a hospital-wide vancomycin-resistant Enterococcus faecium outbreak in France”. Eur J Clin Microbiol Infect Dis. vol. 27. 2008 Nov. pp. 1061-4.

Kurup, A, Chlebicki, MP, Ling, ML, Koh, TH, Tan, KY, Lee, LC, Howe, KB. “Control of a hospital-wide vancomycin-resistant Enterococci outbreak”. Am J Infect Control. vol. 36. 2008 Apr. pp. 206-11.

Tacconelli, E, Cataldo, MA. “Vancomycin-resistant enterococci (VRE): transmission and control”. Int J Antimicrob Agents. vol. 31. 2008 Feb. pp. 99-106.

Deplano, A, Denis, O, Nonhoff, C, Rost, F, Byl, B, Jacobs, F, Vankerckhoven, V, Goossens, H, Struelens, MJ. “Outbreak of hospital-adapted clonal complex-17 vancomycin-resistant Enterococcus faecium strain in a haematology unit: role of rapid typing for early control”. J Antimicrob Chemother. vol. 60. 2007 Oct. pp. 849-54.

Tenover, FC, Swenson, JM, O’Hara, CM, Stocker, SA. “Ability of commercial and reference antimicrobial susceptibility testing methods to detect vancomycin resistance in enterococci”. J Clin Microbiol. vol. 33. 1995 Jun. pp. 1524-7.

Longtin, Y, Sax, H, Allegranzi, B, Schneider, F, Pittet, D. “Videos in clinical medicine. Hand hygiene”. N Engl J Med. vol. 364. 2011 Mar 31. pp. e24

Boyce, JM, Pittet, D. “Healthcare Infection Control Practices Advisory Committee, HICPAC/SHEA/APIC/IDSA Hand Hygiene Task, Force. Guideline for Hand Hygiene in Health-Care Settings. Recommendations of the Healthcare Infection Control Practices Advisory Committee and the HICPAC/SHEA/APIC/IDSA Hand Hygiene Task Force. Society for Healthcare Epidemiology of America/Association for Professionals in Infection Control/Infectious Diseases Society of America”. MMWR Recomm Rep. vol. 51. 2002. pp. 1

Srinivasan, A, Song, X, Ross, T. “A prospective study to determine whether cover gowns in addition to gloves decrease nosocomial transmission of vancomycin-resistant enterococci in an intensive care unit”. Infect Control Hosp Epidemiol. vol. 23. 2002. pp. 424-8.

Puzniak, LA, Leet, T, Mayfield, J. “To gown or not to gown: the effect on acquisition of vancomycin-resistant enterococci”. Clin Infect Dis. vol. 35. 2002. pp. 18-25.

Slaughter, S, Hayden, MK, Nathan, C. “A comparison of the effect of universal use of gloves and gowns with that of glove use alone on acquisition of vancomycin-resistant enterococci in a medical intensive care unit”. Ann Intern Med. vol. 125. 1996. pp. 448-56.

Climo, MW, Sepkowitz, KA, Zuccotti, G. “The effect of daily bathing with chlorhexidine on the acquisition of methicillin-resistant Staphylococcus aureus, vancomycin-resistant Enterococcus, and healthcare-associated bloodstream infections: results of a quasi-experimental multicenter trial”. Crit Care Med. vol. 37. 2009. pp. 1858-65.

Vernon, MO, Hayden, MK, Trick, WE. “Chlorhexidine gluconate to cleanse patients in a medical intensive care unit: the effectiveness of source control to reduce the bioburden of vancomycin-resistant enterococci”. Arch Intern Med. vol. 166. 2006. pp. 306-12.

Jochimsen, EM, Fish, L, Manning, K. “Control of vancomycin-resistant enterococci at a community hospital: efficacy of patient and staff cohorting”. Infect Control Hosp Epidemiol. vol. 20. 1999. pp. 106-9.

Mulin, B, Rouget, C, Clément, C. “Association of private isolation rooms with ventilator-associated Acinetobacter baumanii pneumonia in a surgical intensive-care unit”. Infect Control Hosp Epidemiol. vol. 18. 1997. pp. 499-503.

“Recommendations for preventing the spread of vancomycin resistance”. Infect Control Hosp Epidemiol. vol. 16. 1995 Feb. pp. 105-13.

Weber, SG, Huang, SS, Oriola, S. “Legislative mandates for use of active surveillance cultures to screen for methicillin-resistant Staphylococcus aureus and vancomycin-resistant enterococci: position statement from the Joint SHEA and APIC Task Force”. Infect Control Hosp Epidemiol. vol. 28. 2007. pp. 249-60.

Morgan, DJ, Day, HR, Furuno, JP, Young, A, Johnson, JK, Bradham, DD, Perencevich, EN. “Improving efficiency in active surveillance for methicillin-resistant Staphylococcus aureus or vancomycin-resistant Enterococcus at hospital admission”. Infect Control Hosp Epidemiol. vol. 31. 2010 Dec. pp. 1230-5.

Hachem, R, Graviss, L, Hanna, H. “Impact of surveillance for vancomycin-resistant enterococci on controlling a bloodstream outbreak among patients with hematologic malignancy”. Infect Control Hosp Epidemiol. vol. 25. 2004. pp. 391-4.

Siddiqui, AH, Harris, AD, Hebden, J. “The effect of active surveillance for vancomycin-resistant enterococci in high-risk units on vancomycin-resistant enterococci incidence hospital-wide”. Am J Infect Control. vol. 30. 2002. pp. 40-3.

Singh, N, Léger, MM, Campbell, J. “Control of vancomycin-resistant enterococci in the neonatal intensive care unit”. Infect Control Hosp Epidemiol. vol. 26. 2005. pp. 646-9.

Zirakzadeh, A, Patel, R. “Vancomycin-resistant enterococci: colonization, infection, detection, and treatment”. Mayo Clin Proc. vol. 81. 2006. pp. 529-36.

Hachem, R, Raad, I. “Failure of oral antimicrobial agents in eradicating gastrointestinal colonization with vancomycin-resistant enterococci”. Infect Control Hosp Epidemiol. vol. 23. 2002. pp. 43-4.

Mondy, KE, Shannon, W, Mundy, LM. “Evaluation of zinc bacitracin capsules versus placebo for enteric eradication of vancomycin-resistant Enterococcus faecium”. Clin Infect Dis. vol. 33. 2001. pp. 473-6.

Montecalvo, MA, Horowitz, H, Wormser, GP, Seiter, K, Carbonaro, CA. “Effect of novobiocin-containing antimicrobial regimens on infection and colonization with vancomycin-resistant Enterococcus faecium”. Antimicrob Agents Chemother. vol. 39. 1995 Mar. pp. 794

Weinstein, MR, Dedier, H, Brunton, J, Campbell, I, Conly, JM. “Lack of efficacy of oral bacitracin plus doxycycline for the eradication of stool colonization with vancomycin-resistant Enterococcus faecium”. Clin Infect Dis. vol. 29. 1999 Aug. pp. 361-6.

Wong, MT, Kauffman, CA, Standiford, HC, Linden, P, Fort, G, Fuchs, HJ, Porter, SB, Wenzel, RP. “Effective suppression of vancomycin-resistant Enterococcus species in asymptomatic gastrointestinal carriers by a novel glycolipodepsipeptide, ramoplanin”. Clin Infect Dis. vol. 33. 2001 Nov 1. pp. 1476-82.

Manley, KJ, Fraenkel, MB, Mayall, BC, Power, DA. “Probiotic treatment of vancomycin-resistant enterococci: a randomised controlled trial”. Med J Aust. vol. 186. 2007 May 7. pp. 454-7.

Tacconelli, E, De Angelis, G, Cataldo, MA, Pozzi, E, Cauda, R. “Does antibiotic exposure increase the risk of methicillin-resistant Staphylococcus aureus (MRSA) isolation? A systematic review and meta-analysis”. J Antimicrob Chemother. vol. 61. 2008 Jan. pp. 26-38.

Carling, PC, Bartley, JM. “Evaluating hygienic cleaning in health care settings: what you do not know can harm your patients”. Am J Infect Control. vol. 38. 2010. pp. S41-50.

Williams, VR, Callery, S, Vearncombe, M, Simor, AE. “Utility of environmental sampling for the prevention of transmission of vancomycin resistant enterococci (VRE) in hospitals”. Can J Infect Control. vol. 24. 2009 Summer. pp. 119-24.

Tanner, BD. “Reduction in infection risk through treatment of microbially contaminated surfaces with a novel, portable, saturated steam vapor disinfection system”. Am J Infect Control. vol. 37. 2009. pp. 20-7.

Treatment of enterococcal infections

Arias, CA, Contreras, GA, Murray, BE. “Management of multi-drug resistant enterococcal infections”. Clin Microbiol Infect. vol. 16. 2010. pp. 555-562.

Crank, CW, Scheetz, MH, Brielmaier, B, Rose, WE, Patel, GP, Ritchie, DJ, Segreti, J. “Comparison of outcomes from daptomycin or linezolid treatment for vancomycin-resistant enterococcal bloodstream infection: A retrospective, multicenter, cohort study”. Clin Ther. vol. 32. 2010. pp. 1713-9.

Lai, KK. “Treatment of vancomycin-resistant Enterococcus faecium infections”. Arch Intern Med. vol. 156. 1996. pp. 2579-84.

Chong, YP, Lee, SO, Song, EH, Lee, EJ, Jang, EY, Kim, SH, Choi, SH, Kim, MN, Jeong, JY, Woo, JH, Kim, YS. “Quinupristin-dalfopristin versus linezolid for the treatment of vancomycin-resistant Enterococcus faecium bacteraemia: efficacy and development of resistance”. Scand J Infect Dis. vol. 42. 2010 Jul. pp. 491-9.

Shlaes, DM, Levy, J, Wolinsky, E. “Enterococcal bacteremia without endocarditis”. Arch Intern Med. vol. 141. 1981. pp. 578-81.

Gullberg, RM, Homann, SR, Phair, JP. “Enterococcal bacteremia: analysis of 75 episodes”. Rev Infect Dis. vol. 11. 1989. pp. 74-85.

Hoge, CW, Adams, J, Buchanan, B, Sears, SD. “Enterococcal bacteremia: to treat or not to treat, a reappraisal”. Rev Infect Dis. vol. 13. 1991. pp. 600-5.

Watanakunakorn, C, Patel, R. “Comparison of patients with enterococcal bacteremia due to strains with and without high-level resistance to gentamicin”. Clin Infect Dis. vol. 17. 1993. pp. 74-8.

Gray, J, Marsh, PJ, Stewart, D, Pedler, SJ. “Enterococcal bacteraemia: a prospective study of 125 episodes”. J Hosp Infect. vol. 27. 1994. pp. 179-86.

Baddour, LM, Wilson, WR, Bayer, AS. “Infective endocarditis: diagnosis, antimicrobial therapy, and management of complications: a statement for healthcare professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association: endorsed by the Infectious Diseases Society of America”. Circulation. vol. 111. 2005. pp. e394-434.

“2008 Focused Update Incorporated Into the ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease) Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons”. Journal of the American College of Cardiology. vol. 52. 2008. pp. e1-e142.

Tice, AD. “Short-course therapy of acute cystitis: a brief review of therapeutic strategies”. J Antimicrob Chemother. vol. 43. 1999. pp. 85-93.

Minassian, MA, Lewis, DA, Chattopadhyay, D. “A comparison between single-dose fosfomycin trometamol (Monuril) and a 5-day course of trimethoprim in the treatment of uncomplicated lower urinary tract infection in women”. Int J Antimicrob Agents. vol. 10. 1998. pp. 39-47.

Onrust, SV, Lamb, HM, Balfour, JA. “Ofloxacin. A reappraisal of its use in the management of genitourinary tract infections”. Drugs. vol. 56. 1998. pp. 895-928.

Patel, SS, Balfour, JA, Bryson, HM. “Fosfomycin tromethamine. A review of its antibacterial activity, pharmacokinetic properties and therapeutic efficacy as a single-dose oral treatment for acute uncomplicated lower urinary tract infections”. Drugs. vol. 53. 1997. pp. 637-56.

Corrado, ML, Hesney, M, Struble, WE. “Norfloxacin versus trimethoprim-sulfamethoxazole in the treatment of urinary tract infections”. Eur Urol. vol. 17. 1990. pp. 34-9.

Allerberger, F, Klare, I. “In-vitro activity of fosfomycin against vancomycin-resistant enterococci”. J Antimicrob Chemother. vol. 43. 1999. pp. 211-7.

Homer-Vanniasinkam, S. “Treatment of intra-abdominal and skin and soft tissue infections: the role of the glycylcyclines”. Int J Surg. vol. 4. 2006. pp. 45-52.

Ryan, JL, Pachner, A, Andriole, VT, Root, RK. “Enterococcal meningitis: combined vancomycin and rifampin therapy”. Am J Med. vol. 68. 1980. pp. 449-51.

Elvy, J, Porter, D, Brown, E. “Treatment of external ventricular drain-associated ventriculitis caused by Enterococcus faecalis with intraventricular daptomycin”. J Antimicrob Chemother. vol. 61. 2008. pp. 461-2.

Zeana, C, Kubin, CJ, Della-Latta, P, Hammer, SM. “Vancomycin-resistant Enterococcus faecium meningitis successfully managed with linezolid: case report and review of the literature”. Clin Infect Dis. vol. 33. 2001. pp. 477-82.

Williamson, JC, Glazier, SS, Peacock, JE. “Successful treatment of ventriculostomy-related meningitis caused by vancomycin-resistant Enterococcus with intravenous and intraventricular quinupristin/dalfopristin”. Clin Neurol Neurosurg. vol. 104. 2002. pp. 54-6.

Graham, PL, Ampofo, K, Saiman, L. “Linezolid treatment of vancomycin-resistant Enterococcus faecium ventriculitis”. Pediatr Infect Dis J. vol. 21. 2002. pp. 798-800.


Muto, CA, Jernigan, JA, Ostrowsky, BE. “SHEA guideline for preventing nosocomial transmission of multidrug-resistant strains of Staphylococcus aureus and enterococcus”. Infect Control Hosp Epidemiol. vol. 24. 2003. pp. 362-86.

Cookson, BD, Macrae, MB, Barrett, SP, Brown, DF, Chadwick, C, French, GL, Hateley, P, Hosein, IK, Wade, JJ. “Combined Working Party of the Hospital Infection Society and Infection Control Nurses Association. Guidelines for the control of glycopeptide-resistant enterococci in hospitals”. J Hosp Infect. vol. 62. 2006. pp. 6-21.

Siegel, JD, Rhinehart, E, Jackson, M, Chiarello, L. “Management of multidrug-resistant organisms in healthcare settings”. Centers for Disease Control. 2006.

Clock, SA, Cohen, B, Behta, M, Ross, B, Larson, EL. “Contact precautions for multidrug-resistant organisms: Current recommendations and actual practice”. Am J Infect Control. vol. 38. 2010. pp. 105-11.

Huskins, WC, Huckabee, CM, O’Grady, NP, Murray, P, Kopetskie, H, Zimmer, L. “Intervention to reduce transmission of resistant bacteria in intensive care”. N Engl J Med. vol. 364. 2011. pp. 1407-18.

Bearman, GM, Marra, AR, Sessler, CN, Smith, WR, Rosato, A, Laplante, JK, Wenzel, RP, Edmond, MB. “A controlled trial of universal gloving versus contact precautions for preventing the transmission of multidrug-resistant organisms”. Am J Infect Control. vol. 35. 2007. pp. 650-5.

Mathai, E, Allegranzi, B, Kilpatrick, C, Bagheri Nejad, S, Graafmans, W, Pittet, D. “Promoting hand hygiene in healthcare through national/subnational campaigns”. J Hosp Infect. vol. 77. 2011. pp. 294-8.

Tschudin-Sutter, S, Pargger, H, Widmer, AF. “Hand hygiene in the intensive care unit”. Crit Care Med. vol. 38. 2010. pp. S299-305.

Siegel, JD, Rhinehart, E, Jackson, M, Chiarello, L. “2007 Guideline for Isolation Precautions: Preventing Transmission of Infectious Agents in Healthcare Settings”.

“Options for Evaluation Cleaning”.

“Enterococcus spp. bacteraemia in England, Wales, and Northern Ireland: 2005-2009”.